{"id":4790,"date":"2025-08-25T16:09:05","date_gmt":"2025-08-25T20:09:05","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=4790"},"modified":"2025-12-13T17:53:48","modified_gmt":"2025-12-13T22:53:48","slug":"neural-and-hormonal-regulation-of-blood-pressure","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/neural-and-hormonal-regulation-of-blood-pressure\/","title":{"raw":"7p11 Neural and Hormonal Regulation of Blood Pressure","rendered":"7p11 Neural and Hormonal Regulation of Blood Pressure"},"content":{"raw":"The body uses both neural<\/strong> and hormonal mechanisms<\/strong> to control systemic blood pressure<\/strong> and cardiac output.<\/strong>\r\n\r\nBoth neural and hormonal regulation mechanisms are required in order to maintain adequate perfusion throughout the body, in a manner that is responsive to various daily activities (e.g., standing up, sitting down, running, thinking hard etc.)\r\n

Blood Pressure Homeostasis Regulatory Mechanisms:<\/strong><\/h1>\r\n
    \r\n \t
  • Chemoreceptors<\/strong> and Baroreceptors<\/strong> in the carotid sinus and aortic arch monitor blood oxygen and pressure.\u00a0 Chemoreceptors<\/strong> are also located on the ventrolateral surface of the medulla oblongata.<\/li>\r\n \t
  • Chemoreceptors:<\/strong> monitor blood levels of O2<\/sub>, CO2<\/sub> and pH.<\/li>\r\n \t
  • Baroreceptors:<\/strong> monitor blood pressure in the carotid sinus and aortic arch.<\/li>\r\n<\/ul>\r\n \r\n
      \r\n \t
    • The medulla oblongata<\/strong> uses that information to adjust heart rate, heart contractility (force of contraction),<\/strong> and vascular tone<\/strong> to stabilize blood pressure.\r\n
        \r\n \t
      • Adjustments made by the brain (cardiovascular centers in the medulla oblongata):<\/strong>\r\n
          \r\n \t
        • Heart Rate:<\/strong> Speeds up or slows down (via sympathetic or parasympathetic pathways respectively)<\/li>\r\n \t
        • Force of Contraction:<\/strong> Increases or decreases (via sympathetic or parasympathetic pathways respectively), which modulates stroke volume.<\/li>\r\n \t
        • Vascular Tone:<\/strong> Vasocontrict (via sympathetic pathway) or vasodilate to adjust resistance and blood flow.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n \r\n
            \r\n \t
          • The body constantly makes adjustments to heart rate, stroke volume,<\/strong> and vascular tone<\/strong> (vasodilation\/vasoconstriction), to ensure tissues receive sufficient blood, oxygen, and nutrients and can also facilitate the removal of waste products produced by cells.<\/li>\r\n<\/ul>\r\n

            Sympathetic Response (\"Fight or Flight\")<\/strong><\/h1>\r\n
              \r\n \t
            • Via Cardiac Accelerator Nerve <\/strong>releasing n<\/strong>eurotransmitters:<\/strong>\r\n
                \r\n \t
              • Epinephrine (E) and norepinephrine (NE)<\/strong> are released and bind to:<\/li>\r\n \t
              • Beta-1 adrenergic receptors<\/strong> on the Sinoatrial (SA) node, which opens more Ca++<\/sup> channels, bringing cardiomyocytes closer to threshold:\r\n
                  \r\n \t
                • Increase depolarization rate, speeding heart rate (\"beat\" the heart faster).<\/li>\r\n \t
                • Increase force of contraction (positive inotropy).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                • Alpha-1 adrenergic receptors<\/strong>\u00a0in arteries:\r\n
                    \r\n \t
                  • Cause vasoconstriction, increasing resistance and BP.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                  • Memory trick:<\/strong>\r\n
                      \r\n \t
                    • A's for a<\/span>lpha-1 a<\/span>drenergic receptors in a<\/span>rterial walls<\/em>\u00a0(vasoconstriction).<\/li>\r\n \t
                    • B's for b<\/span>eta in the b<\/span>eating heart<\/em>\u00a0(speeding heart rate).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

                      Parasympathetic Response (\"Rest and Digest\")<\/strong><\/h1>\r\n
                        \r\n \t
                      • Via\u00a0vagus nerve (cranial nerve X)<\/strong>:\r\n
                          \r\n \t
                        • Releases\u00a0acetylcholine (ACh)<\/strong> which bind to muscarinic receptors<\/strong> in the SA node.<\/li>\r\n \t
                        • Stimulating the opening of potassium channels<\/strong>, hyperpolarizing cells, which slows depolarization and decreases HR<\/strong>.<\/li>\r\n \t
                        • Reduces force of contraction (heart contractility)<\/strong> and overall cardiac output.<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

                          Heart Medications that Modulate Heart Rate and Contractility<\/h1>\r\nBeta-adrenergic Receptors and Beta-Blocker Drugs:<\/strong>\r\n
                            \r\n \t
                          • Beta-1 adrenergic receptors<\/strong>: Located in the SA node of the heart.<\/li>\r\n \t
                          • Beta-blockers<\/strong>: Drugs that\u00a0block<\/strong>\u00a0these receptors, preventing sympathetic stimulation.<\/li>\r\n \t
                          • Function of beta-1 blockade<\/strong>:\r\n
                              \r\n \t
                            • Prevents epinephrine\/norepinephrine from increasing heart rate and contractility.<\/li>\r\n \t
                            • Result: Slower heart rate and reduced force of contraction, giving the heart a \u201crest\u201d to recover, especially beneficial in damaged hearts.\u00a0 However, can mean that person becomes more exercise-intolerant (unable to elevate heart rate and contractility required for moderate-vigourous physical activity), a condition that can be desirable if a person's heart is damaged or has reduced perfusion due to blocked\/narrowed coronary arteries.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                            • In contrast,\u00a0beta-2 adrenergic receptors<\/strong> are in other tissues (like bronchioles), but they are not targeted in cardiovascular therapies.\u00a0 This is beneficial as sympathetic-induced bronchodilation via epinephrine\/norepinephrine is still possible.<\/li>\r\n<\/ul>\r\n \r\n\r\nBlood Volume Regulation and Hormones<\/strong>\r\n
                                \r\n \t
                              • Blood volume influences BP proportionality:<\/strong>\r\n
                                  \r\n \t
                                • Increased volume elevates BP; decreased volume lowers BP.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                • Kidneys:<\/strong>\r\n
                                    \r\n \t
                                  • Responsible for regulating blood volume via urine output.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                  • Antidiuretic hormone (ADH):<\/strong>\r\n
                                      \r\n \t
                                    • Increases blood volume<\/strong>\u00a0by promoting water reabsorption in kidneys.<\/li>\r\n \t
                                    • Causes vasoconstriction, raising BP.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                    • Aldosterone:<\/strong>\r\n
                                        \r\n \t
                                      • Promotes salt and water retention, increasing blood volume and BP.<\/li>\r\n \t
                                      • Decreases urine output.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                      • Renin-Angiotensin System:<\/strong>\r\n
                                          \r\n \t
                                        • When BP drops, kidneys release\u00a0renin<\/strong>.<\/li>\r\n \t
                                        • Renin converts\u00a0angiotensinogen<\/strong> into angiotensin I<\/li>\r\n \t
                                        • ACE (Angiotensin Converting Enzyme) is released from the lungs and converts angiotensin I into the active form angiotensin II<\/li>\r\n \t
                                        • Angiotensin II stimulates the release of Aldosterone<\/strong> from the adrenal cortex<\/li>\r\n \t
                                        • Angiotensin II stimulates the release of Antidiuretic Hormone<\/strong> (ADH) from the posterior pituitary gland.<\/li>\r\n \t
                                        • Aldosterone and ADH stimulate water and salt reabsorption leading to an increase in blood volume and blood pressure.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>","rendered":"

                                          The body uses both neural<\/strong> and hormonal mechanisms<\/strong> to control systemic blood pressure<\/strong> and cardiac output.<\/strong><\/p>\n

                                          Both neural and hormonal regulation mechanisms are required in order to maintain adequate perfusion throughout the body, in a manner that is responsive to various daily activities (e.g., standing up, sitting down, running, thinking hard etc.)<\/p>\n

                                          Blood Pressure Homeostasis Regulatory Mechanisms:<\/strong><\/h1>\n
                                            \n
                                          • Chemoreceptors<\/strong> and Baroreceptors<\/strong> in the carotid sinus and aortic arch monitor blood oxygen and pressure.\u00a0 Chemoreceptors<\/strong> are also located on the ventrolateral surface of the medulla oblongata.<\/li>\n
                                          • Chemoreceptors:<\/strong> monitor blood levels of O2<\/sub>, CO2<\/sub> and pH.<\/li>\n
                                          • Baroreceptors:<\/strong> monitor blood pressure in the carotid sinus and aortic arch.<\/li>\n<\/ul>\n

                                             <\/p>\n

                                              \n
                                            • The medulla oblongata<\/strong> uses that information to adjust heart rate, heart contractility (force of contraction),<\/strong> and vascular tone<\/strong> to stabilize blood pressure.\n
                                                \n
                                              • Adjustments made by the brain (cardiovascular centers in the medulla oblongata):<\/strong>\n
                                                  \n
                                                • Heart Rate:<\/strong> Speeds up or slows down (via sympathetic or parasympathetic pathways respectively)<\/li>\n
                                                • Force of Contraction:<\/strong> Increases or decreases (via sympathetic or parasympathetic pathways respectively), which modulates stroke volume.<\/li>\n
                                                • Vascular Tone:<\/strong> Vasocontrict (via sympathetic pathway) or vasodilate to adjust resistance and blood flow.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                                   <\/p>\n

                                                    \n
                                                  • The body constantly makes adjustments to heart rate, stroke volume,<\/strong> and vascular tone<\/strong> (vasodilation\/vasoconstriction), to ensure tissues receive sufficient blood, oxygen, and nutrients and can also facilitate the removal of waste products produced by cells.<\/li>\n<\/ul>\n

                                                    Sympathetic Response (“Fight or Flight”)<\/strong><\/h1>\n
                                                      \n
                                                    • Via Cardiac Accelerator Nerve <\/strong>releasing n<\/strong>eurotransmitters:<\/strong>\n
                                                        \n
                                                      • Epinephrine (E) and norepinephrine (NE)<\/strong> are released and bind to:<\/li>\n
                                                      • Beta-1 adrenergic receptors<\/strong> on the Sinoatrial (SA) node, which opens more Ca++<\/sup> channels, bringing cardiomyocytes closer to threshold:\n
                                                          \n
                                                        • Increase depolarization rate, speeding heart rate (“beat” the heart faster).<\/li>\n
                                                        • Increase force of contraction (positive inotropy).<\/li>\n<\/ul>\n<\/li>\n
                                                        • Alpha-1 adrenergic receptors<\/strong>\u00a0in arteries:\n
                                                            \n
                                                          • Cause vasoconstriction, increasing resistance and BP.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n
                                                          • Memory trick:<\/strong>\n
                                                              \n
                                                            • A’s for a<\/span>lpha-1 a<\/span>drenergic receptors in a<\/span>rterial walls<\/em>\u00a0(vasoconstriction).<\/li>\n
                                                            • B’s for b<\/span>eta in the b<\/span>eating heart<\/em>\u00a0(speeding heart rate).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                                              Parasympathetic Response (“Rest and Digest”)<\/strong><\/h1>\n
                                                                \n
                                                              • Via\u00a0vagus nerve (cranial nerve X)<\/strong>:\n
                                                                  \n
                                                                • Releases\u00a0acetylcholine (ACh)<\/strong> which bind to muscarinic receptors<\/strong> in the SA node.<\/li>\n
                                                                • Stimulating the opening of potassium channels<\/strong>, hyperpolarizing cells, which slows depolarization and decreases HR<\/strong>.<\/li>\n
                                                                • Reduces force of contraction (heart contractility)<\/strong> and overall cardiac output.<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                                                  Heart Medications that Modulate Heart Rate and Contractility<\/h1>\n

                                                                  Beta-adrenergic Receptors and Beta-Blocker Drugs:<\/strong><\/p>\n

                                                                    \n
                                                                  • Beta-1 adrenergic receptors<\/strong>: Located in the SA node of the heart.<\/li>\n
                                                                  • Beta-blockers<\/strong>: Drugs that\u00a0block<\/strong>\u00a0these receptors, preventing sympathetic stimulation.<\/li>\n
                                                                  • Function of beta-1 blockade<\/strong>:\n
                                                                      \n
                                                                    • Prevents epinephrine\/norepinephrine from increasing heart rate and contractility.<\/li>\n
                                                                    • Result: Slower heart rate and reduced force of contraction, giving the heart a \u201crest\u201d to recover, especially beneficial in damaged hearts.\u00a0 However, can mean that person becomes more exercise-intolerant (unable to elevate heart rate and contractility required for moderate-vigourous physical activity), a condition that can be desirable if a person’s heart is damaged or has reduced perfusion due to blocked\/narrowed coronary arteries.<\/li>\n<\/ul>\n<\/li>\n
                                                                    • In contrast,\u00a0beta-2 adrenergic receptors<\/strong> are in other tissues (like bronchioles), but they are not targeted in cardiovascular therapies.\u00a0 This is beneficial as sympathetic-induced bronchodilation via epinephrine\/norepinephrine is still possible.<\/li>\n<\/ul>\n

                                                                       <\/p>\n

                                                                      Blood Volume Regulation and Hormones<\/strong><\/p>\n

                                                                        \n
                                                                      • Blood volume influences BP proportionality:<\/strong>\n
                                                                          \n
                                                                        • Increased volume elevates BP; decreased volume lowers BP.<\/li>\n<\/ul>\n<\/li>\n
                                                                        • Kidneys:<\/strong>\n
                                                                            \n
                                                                          • Responsible for regulating blood volume via urine output.<\/li>\n<\/ul>\n<\/li>\n
                                                                          • Antidiuretic hormone (ADH):<\/strong>\n
                                                                              \n
                                                                            • Increases blood volume<\/strong>\u00a0by promoting water reabsorption in kidneys.<\/li>\n
                                                                            • Causes vasoconstriction, raising BP.<\/li>\n<\/ul>\n<\/li>\n
                                                                            • Aldosterone:<\/strong>\n
                                                                                \n
                                                                              • Promotes salt and water retention, increasing blood volume and BP.<\/li>\n
                                                                              • Decreases urine output.<\/li>\n<\/ul>\n<\/li>\n
                                                                              • Renin-Angiotensin System:<\/strong>\n
                                                                                  \n
                                                                                • When BP drops, kidneys release\u00a0renin<\/strong>.<\/li>\n
                                                                                • Renin converts\u00a0angiotensinogen<\/strong> into angiotensin I<\/li>\n
                                                                                • ACE (Angiotensin Converting Enzyme) is released from the lungs and converts angiotensin I into the active form angiotensin II<\/li>\n
                                                                                • Angiotensin II stimulates the release of Aldosterone<\/strong> from the adrenal cortex<\/li>\n
                                                                                • Angiotensin II stimulates the release of Antidiuretic Hormone<\/strong> (ADH) from the posterior pituitary gland.<\/li>\n
                                                                                • Aldosterone and ADH stimulate water and salt reabsorption leading to an increase in blood volume and blood pressure.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n","protected":false},"author":1370,"menu_order":17,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-4790","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":55,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4790","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":14,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4790\/revisions"}],"predecessor-version":[{"id":5579,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4790\/revisions\/5579"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/55"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4790\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=4790"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=4790"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=4790"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=4790"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}