Physiology of Blood Pressure Regulation

Physiologic Regulation of Blood Pressure

• Blood pressure (BP) is regulated through complex physiological mechanisms involving neural and hormonal pathways.
• Baroreceptors, located in major arteries, detect changes in BP by sensing arterial wall stretch and initiate reflex responses to maintain homeostasis.

Heart Rate and Cardiac Output

• Heart rate (HR) and stroke volume (SV) determine cardiac output (CO); CO = HR x SV, crucial for blood circulation.
• Endogenous regulation includes:
  • Parasympathetic nerves: Slow heart rate via acetylcholine release.
  • Sympathetic nerves: Increase heart rate and contractility via norepinephrine.
  • Renin-Angiotensin-Aldosterone System (RAAS): Raises BP and regulates fluid balance.
  • Endothelium-derived factors: Nitric oxide promotes vasodilation, affecting vascular tone.

Impact of Preload and Afterload on BP

• Preload: The initial stretching of the cardiac muscle before contraction; influenced by venous return.
• Afterload: The resistance the heart must overcome to eject blood; determined by arterial pressure and vessel diameter.
• Increased CO raises BP; both preload and afterload significantly influence ventricular function and systemic BP.

Factors Determining Preload, Afterload, and Cardiac Output

• Preload is influenced by blood volume and venous return.
• Afterload is influenced by systemic vascular resistance and arterial elasticity.
• Cardiac output is determined by heart rate, stroke volume, and contractility of the heart.

Role of the Kidneys in Regulating BP

• Kidneys regulate BP through:
  • Fluid balance: Adjusting blood volume.
  • RAAS activation: Controlling sodium and water reabsorption, influencing blood volume and vascular resistance.

Endogenous Processes in Hypertension Pathophysiology

• Hypertension (HTN) may result from overactivity of RAAS, endothelial dysfunction, or increased sympathetic nervous system activity, leading to persistent elevation in BP.

Major Drug Classes in HTN Treatment

• Diuretics: Reduce blood volume; act on kidneys to promote salt and water excretion.
• ACE inhibitors: Block angiotensin II production; lower vasoconstriction.
• ARBs: Block angiotensin II receptors; reduce vasoconstriction and promote vasodilation.
• Calcium Channel Blockers: Impair calcium entry into muscle cells; decrease contractility and promote vasodilation.
• Beta-blockers: Reduce heart rate and myocardial contractility.

Predicting Drug Effects on BP

• Understanding pharmacological actions helps predict effects on BP; for example, ACE inhibitors decrease afterload and preload without significantly affecting HR or SV.
• Vasodilators typically lower afterload but can also influence preload depending on their mechanism of action.

Antihypertensive Drugs and Baroreceptor Reflex

• Some antihypertensive drugs may induce reflex tachycardia by activating baroreceptors in response to sudden BP drops, which stimulates the sympathetic nervous system.

Vasodilators and Preload, Afterload Impact

• Depending on specific vasodilators, effects can vary; drugs targeting arterial smooth muscle primarily lower afterload, while those affecting venous capacitance may decrease preload.

Physiologic Regulation of Blood Pressure

• Blood pressure (BP) is regulated through complex physiological mechanisms involving neural and hormonal pathways.
• Baroreceptors, located in major arteries, detect changes in BP by sensing arterial wall stretch and initiate reflex responses to maintain homeostasis.

Heart Rate and Cardiac Output

• Heart rate (HR) and stroke volume (SV) determine cardiac output (CO); CO = HR x SV, crucial for blood circulation.
• Endogenous regulation includes:
  • Parasympathetic nerves: Slow heart rate via acetylcholine release.
  • Sympathetic nerves: Increase heart rate and contractility via norepinephrine.
  • Renin-Angiotensin-Aldosterone System (RAAS): Raises BP and regulates fluid balance.
  • Endothelium-derived factors: Nitric oxide promotes vasodilation, affecting vascular tone.

Impact of Preload and Afterload on BP

• Preload: The initial stretching of the cardiac muscle before contraction; influenced by venous return.
• Afterload: The resistance the heart must overcome to eject blood; determined by arterial pressure and vessel diameter.
• Increased CO raises BP; both preload and afterload significantly influence ventricular function and systemic BP.

Factors Determining Preload, Afterload, and Cardiac Output

• Preload is influenced by blood volume and venous return.
• Afterload is influenced by systemic vascular resistance and arterial elasticity.
• Cardiac output is determined by heart rate, stroke volume, and contractility of the heart.

Role of the Kidneys in Regulating BP

• Kidneys regulate BP through:
  • Fluid balance: Adjusting blood volume.
  • RAAS activation: Controlling sodium and water reabsorption, influencing blood volume and vascular resistance.

Endogenous Processes in Hypertension Pathophysiology

• Hypertension (HTN) may result from overactivity of RAAS, endothelial dysfunction, or increased sympathetic nervous system activity, leading to persistent elevation in BP.

Major Drug Classes in HTN Treatment

• Diuretics: Reduce blood volume; act on kidneys to promote salt and water excretion.
• ACE inhibitors: Block angiotensin II production; lower vasoconstriction.
• ARBs: Block angiotensin II receptors; reduce vasoconstriction and promote vasodilation.
• Calcium Channel Blockers: Impair calcium entry into muscle cells; decrease contractility and promote vasodilation.
• Beta-blockers: Reduce heart rate and myocardial contractility.

Predicting Drug Effects on BP

• Understanding pharmacological actions helps predict effects on BP; for example, ACE inhibitors decrease afterload and preload without significantly affecting HR or SV.
• Vasodilators typically lower afterload but can also influence preload depending on their mechanism of action.

Antihypertensive Drugs and Baroreceptor Reflex

• Some antihypertensive drugs may induce reflex tachycardia by activating baroreceptors in response to sudden BP drops, which stimulates the sympathetic nervous system.

Vasodilators and Preload, Afterload Impact

• Depending on specific vasodilators, effects can vary; drugs targeting arterial smooth muscle primarily lower afterload, while those affecting venous capacitance may decrease preload.