ANS Control of Blood Pressure

ANS Control of Blood Pressure

• The autonomic nervous system (ANS) modulates blood pressure through the sympathetic (SNS) and parasympathetic (PNS) systems.
• The SNS increases blood pressure through vasoconstriction, increased heart rate, and increased contractility.
• The PNS decreases blood pressure through decreased heart rate.

Chronic Control of Blood Pressure

• The renin-angiotensin-aldosterone system (RAAS) regulates blood volume and thus blood pressure in the long term.
• Anti-diuretic hormone (ADH) plays a key role in regulating blood volume.
• Natriuretic peptides (NPs) act to decrease blood volume and blood pressure.

Baroreceptors and Blood Pressure

• Baroreceptors monitor blood pressure and signal to the brain to adjust the SNS and PNS activity.
• Decreases in blood pressure cause an increase in SNS activity and decreases in PNS activity.
• Increases in blood pressure cause a decrease in SNS activity and increases in PNS activity.

SNS and PNS Control of BP

• SNS increases cardiac output (CO) by effects on the heart and veins, and increases systemic vascular resistance (SVR) to maintain pressure.
• PNS activation has major effects on the heart to decrease CO.

Long-Term BP Control/Regulation

• Several physiological mechanisms regulate long-term blood pressure by regulating blood volume.
• These systems include the RAAS, ADH, and NPs.

Short and Long-Term Response to Low BP or Blood Volume

• Short-term response is mediated by sympathetic activation of adrenal gland causing release of epinephrine/norepinephrine leading to an increased cardiac output and peripheral vasoconstriction.
• Long-term response includes the activation of Renin and Erythropoietin from the kidneys, leading to an increased erythrocyte (RBC) formation and increased blood volume.

RAAS System

• Renin is produced by the kidney.
• Angiotensinogen is cleaved to Ang I.
• Angiotensin I is converted to Ang II (in the lungs) by ACE.
• Ang II increases blood pressure by:
  • Increasing vasoconstriction
  • Increasing blood volume by stimulating ADH and aldosterone release
• Aldosterone increases Na+ reabsorption in the kidney, further increasing blood volume and pressure.

CNS Control of Blood Pressure

• CNS integrates inputs from baroreceptors in the heart and blood vessels.
• The CNS regulates the output of the sympathetic and parasympathetic nervous systems to maintain relatively stable blood pressure.
• CNS can stimulate RAAS for long-term changes in blood pressure.

Juxtaglomerular Cells and Renin Release

• Juxtaglomerular cells in the kidneys release renin in response to sympathetic stimulation.
• Renin activates the RAAS pathway to increase blood pressure.

Angiotensin II and Effects on the Kidneys

• Angiotensin II directly increases Na+ transporters in proximal tubules.
• Angiotensin II increases ENaC (epithelial Na channel) in cortical collecting duct to increase Na+ reabsorption.

Angiotensin II and Vasoconstriction

• Angiotensin II is a potent vasoconstrictor.
• Its effects are mediated by activation of AT1 receptors, calcium,phospholipase C and RhoA/ROCK pathways.

Aldosterone Release from Adrenal Cortex

• Cells of the adrenal cortex have AT1 receptors.
• Angiotensin II stimulates aldosterone release.
• Aldosterone's main function is to increase sodium reabsorption in kidneys leading to water reabsorption.

Ang II and ADH (Vasopressin) Release

• Angiotensin II stimulates ADH (vasopressin) release by affecting receptors in the hypothalamus.
• ADH acts by increasing water reabsorption in the kidneys.

Angiotensin II Effects: Kidney and Salt

• Angiotensin II triggers vasoconstriction leading to increased blood pressure.
• Reduced renal perfusion and tubular Na reabsorption increase H₂O retention.

Ang II and SNS Summary

• Elevated SNS activity increases renin release through beta-AR stimulation in the kidney.
• Ang II causes an increase in Na+ reabsorption in the kidneys resulting in increases in blood volume and pressure.

Natriuretic Peptides

• A class of peptides that cause excretion of sodium from the tubules, resulting in decreased blood volume and blood pressure.
• ANP is produced in the atria, BNP in the ventricles, and C-type NPs in the vasculature.

NP Receptors and Vessels

• NPRA and NPRB receptors have guanylate cyclase built in.
• cGMP production leads to PKG activation which promotes vasodilation.

NP Effects on Kidney

• NPs oppose the RAAS pathways.
• They promote Na+ excretion, decrease blood pressure, and cause afferent dilation of the glomerular filtration rate, and consequent decrease in blood volume.

NPs, SNS, and RAAS

• NPs antagonize RAAS and SNS signaling, reducing SNS effects on kidney and blood vessels, and affecting CNS regulation of these pathways.

NP Effects and Blood Pressure Regulation

• NPs are produced by heart and regulate blood pressure and sodium reabsorption through actions on blood vessels, the kidney, and CNS.
• NPs cause vasodilation to decrease blood pressure

BP Regulation: Response if BP Low

• Acute responses involve baroreceptors, increase in sympathetic nervous activity, and release of epinephrine.
• Chronic responses involve SNS activation, renin production, aldosterone and ADH release.

Responses if BP High

• Acute responses involve baroreceptor stimulation, decrease in sympathetic nerve activity, increasing parasympathetic stimulation, decrease in vasoconstriction and increase in Na excretion.
• Chronic responses involve stretch on the heart activating ANP & BNP and increase in Na excretion, reducing SNS and RAAS activity.

SNS Activity and Control

• The sympathetic nervous system (SNS) activity has a continuous output, which is called 'sympathetic tone'.
• Increases/decreases in SNS activity, which can be controlled by baroreceptors, leads to changes in blood pressure.

α and β Adrenergic Receptors

• Alpha adrenergic receptors are located on vascular smooth muscle and cause vasoconstriction.
• Beta adrenergic receptors are primarily found on the heart leading to increases in cardiac rate and contractility.

β-agonists and their Selectivity

• β-agonists can be selective for one or more types of adrenergic receptors, influencing which responses are greater.
• Examples include epinephrine, norepinephrine, dopamine, dobutamine, and isoproterenol.

Norepinephrine Infusion

• Norepinephrine stimulates α1 and β1 adrenergic receptors.
• The effects include an increase in heart rate, blood pressure, and vasoconstriction.
• Baroreceptor response leads to short-term changes, while prolonged infusion causes sustained effects.

Epinephrine Infusion and Blood Pressure

• At low doses, epinephrine acts as a ß1 and ß2 agonist, leading to vasodilation, increased heart rate and cardiac output, and lowered blood pressure.
• High doses of epinephrine causes a stronger vasoconstriction response due stimulation of α1 adrenergic receptors leading to an increased blood pressure.

Example of Phenylephrine Infusion

• Phenylephrine is a pure alpha agonist.
• Increasing blood pressure causes a decrease in heart rate due to baroreceptor activation.
• Infusion may have a greater increase in blood pressure if the baroreceptor pathway is blocked.

SNS Activity is Controlled by AR Signaling

• SNS can be influenced by different adrenergic receptors (alpha and beta).
• Different adrenergic receptor subtypes exist that act differently to evoke various physiological outcomes.

Summary / Things to Know

• Understanding the mechanisms of SNS activation of RAAS, ADH, and aldosterone for increasing blood pressure.
• The role of Natriuretic Peptides in decreasing blood pressure.

This quiz explores the autonomic nervous system's (ANS) role in regulating blood pressure through its sympathetic and parasympathetic branches. It covers the chronic control mechanisms involving the renin-angiotensin-aldosterone system, baroreceptors, and the effects of various hormones. Test your knowledge on how these systems interact to maintain cardiovascular stability.