Pharmacology: Minoxidil and Hydralazine Effects

Minoxidil relaxes vascular smooth muscle in arterioles, causing peripheral vasodilation.

Minoxidil's vasodilation triggers a reflex increase in heart rate due to the sympathetic nervous system (SNS).

Minoxidil also increases the heart's pumping strength (contractility) due to the SNS.

Minoxidil can cause headache, palpitations, flushing, and fluid retention, due to the RAA pathway activation.

In patients with heart problems, minoxidil's reflex tachycardia and sympathetic stimulation can worsen angina or create irregular heartbeats.

A class of drugs commonly used to lower blood pressure by inhibiting the enzyme ACE (angiotensin-converting enzyme), which leads to decreased angiotensin II (A-II) production.

A powerful vasoconstrictor produced in the body. It causes blood vessels to narrow, increasing blood pressure.

ACEIs reduce blood pressure by decreasing total peripheral resistance (TPR). They do this by promoting vasodilation (widening of blood vessels) and lowering A-II levels.

ACEIs increase bradykinin levels. Bradykinin is a vasodilator, further contributing to blood pressure lowering.

A common side effect of ACEIs is a dry, persistent cough. This is thought to be related to increased bradykinin levels.

Angioedema, a serious, potentially fatal swelling in the face, neck, tongue, or airway, can occur with ACE inhibitors.

ACE inhibitors increase kinin levels, contributing to angioedema and potentially causing renal problems.

Patients with bilateral renal artery stenosis are at increased risk of renal failure when taking ACE inhibitors.

ACE inhibitors are contraindicated during pregnancy due to potential fetal harm.

ACE inhibitors improve cardiac output and survival in patients with heart failure.

ACE inhibitors reduce the progression of diabetic nephropathy and the need for dialysis in diabetic patients.

ARBs have similar effects to ACEIs but work differently, targeting angiotensin receptors directly.

ARBs don't affect bradykinin metabolism, making them more selective in blocking angiotensin effects than ACEIs.

Angiotensin Receptor Blockers (ARBs) are medications that block the action of angiotensin II, a hormone that causes blood vessels to constrict. This helps lower blood pressure.

ARBs selectively block AT1 receptors, found in various tissues. This reduces vasoconstriction, aldosterone secretion, and sodium/water reabsorption, all contributing to lower blood pressure.

Common ARBs include irbesartan (Avapro), losartan (Cozaar), valsartan (Diovan), candesartan (Atacand), olmesartan (Benicar), eprosartan (Teveten), and telmisartan (Micardis).

Direct Renin Inhibitors (DRIs) are a class of medications that directly block the renin enzyme, preventing the formation of angiotensin I, which is a precursor to angiotensin II.

The only currently available DRI is aliskiren (Tekturna).

DRIs have similar side effects as ARBs (less risk of cough and angioedema). They are not recommended in pregnancy.

Calcium Channel Blockers (CCBs) are medications that help lower blood pressure by reducing the amount of calcium that enters the cells of the heart and blood vessels.

CCBs inhibit calcium influx into arterial smooth muscle and cardiac muscle and nodal cells, leading to relaxation of the blood vessels and a decrease in heart rate, ultimately lowering blood pressure.