Blood Pressure Regulation: Short-Term & Long-Term Control

Blood Pressure, Renal Control, and Hypertension

• Blood pressure regulation involves both short-term and long-term mechanisms.
• Short-term regulation is primarily controlled by the baroreceptor reflex
• Baroreceptors in the carotid sinus and aortic arch detect changes in arterial pressure.
• Increased pressure stretches these receptors, triggering signals to the medulla oblongata.
• Signals are sent through the glossopharyngeal and vagus nerves and affect the heart which reduces heart rate and cardiac output, it also causes vasodilation in the blood vessels. Reducing total peripheral resistance (TPR).
• This quick response helps maintain homeostasis but does not control sustained increases in blood pressure.
• Long-term regulation of blood pressure involves several neurohormonal factors.
• The renin-angiotensin-aldosterone system, sympathetic nervous system, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP) play crucial roles

Objectives

• Understand the roles of various body systems in controlling blood pressure.
• Know the function of the sympathetic nervous system, renin-angiotensin-aldosterone (RAA) system, ADH, and ANP in blood pressure regulation.
• Define and understand different types of hypertension.
• Identify the primary groups of drugs used to treat hypertension, and understand their mechanism of action.

Neurohormonal Factors

• Four neurohormonal factors regulate blood pressure: renin-angiotensin-aldosterone system, sympathetic nervous system, ADH, and ANP.
• These factors interact to control sodium balance and extracellular fluid (ECF) volume.

Baroreceptor Reflex

• The baroreceptor reflex quickly responds to acute blood pressure changes.
• A 5–10% drop in blood pressure triggers low-pressure baroreceptors in the heart and lungs to signal the medulla, resulting in ADH secretion, lowered ANP release, and sympathetic nerve outflow.
• A 5–150% change in blood pressure triggers signals through vagus and glossopharyngeal nerves, decreasing sympathetic nerve activity and ADH secretion.

Sympathetic Nervous System

• The sympathetic nervous system plays a role in long-term pressure regulation.
• Vasoconstriction by α1-adrenoceptors, increased heart rate and contractility by β1-adrenoceptors, decreased renal blood flow, reduced glomerular filtration rate (GFR), and sodium excretion, and increased renin release from juxtaglomerular cells are effects of this system.
• Increased levels of angiotensin II and aldosterone are produced.

Antidiuretic Hormone (ADH)

• ADH's actions include increasing aquaporin presence in the collecting duct of the kidneys, increasing water reabsorption, and producing concentrated urine.
• Its release is stimulated by increases in plasma osmolarity or hypovolemia. It also causes vasoconstriction reducing losses and maintaining the blood volume

Atrial Natriuretic Peptide (ANP)

• ANP acts opposite to other regulators, promoting sodium excretion.
• Synthesised in atrial myocytes.
• Released in response to high blood pressure, leading to vasodilation of afferent arterioles and increases in Na+ loss in the urine and a reduced blood volume.
• Reduced blood pressure causes a reduced ANP release.

Prostaglandins

• Prostaglandins are vasodilators, mainly PGE2.
• They enhance glomerular filtration and reduce sodium reabsorption.
• They act as a buffer against excessive vasoconstriction by the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS).

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

• NSAIDs inhibit the enzymes that produce prostaglandins and therefore negatively affect the kidneys, leading to decreased blood flow and GFR and exacerbates heart failure and or hypertension.

Renin-Angiotensin System

• Reduced kidney perfusion pressure activates renin release from juxtaglomerular cells.
• Renin converts angiotensinogen to angiotensin I, then to angiotensin II by ACE.
• Angiotensin II is a potent vasoconstrictor and stimulates aldosterone release.
• Reduced NaCl concentration in the macula densa and sympathetic stimulation trigger renin release.

Angiotensin II

• Angiotensin II is a potent vasoconstrictor that increases total peripheral resistance (TPR).
• It causes vasoconstriction of afferent and efferent arterioles.
• Stimulates aldosterone release, leading to increased sodium and water reabsorption.
• It stimulates sympathetic activity, the thirst mechanism, and ADH release from the hypothalamus.

Hypertension

• Persistent high blood pressure (systolic ≥ 140 mmHg and/or diastolic ≥ 90 mmHg).
• Two main types: essential (cause unknown, 95% of cases) & secondary (known cause e.g.: Renovascular disease, chronic renal disease, hyperaldosteronism, Cushing's syndrome).

Hypertension Complications

• Increased afterload causing left ventricle hypertrophy and increased myocardial demand.
• Increased risk of angina and MI, arrhythmia, and heart failure as a result of arterial damage including atherosclerosis, weakened blood vessels, aneuryms, renal failure and retinopathy.

Treatment of Hypertension

• ACE inhibitors: Inhibit ACE to prevent angiotensin II production.

• Angiotensin II receptor antagonists: Block angiotensin II action.

• Thiazide diuretics: Inhibit sodium-chloride cotransporter in distal renal tubules promoting sodium and water loss.

• Calcium channel blockers: Reduce calcium influx into smooth muscle, causing vasodilation.

• β-blockers: Block β1-receptors, reducing heart rate and contractility.

Explore short-term blood pressure control via the baroreceptor reflex and long-term regulation involving the renin-angiotensin-aldosterone system, sympathetic nervous system, ADH, and ANP. Understand how these neurohormonal factors maintain blood pressure homeostasis.