Hypoglycemia.

Weight gain.

Hyperglycemia.

Bronchospasm.

Lipodystrophy.

Both types are equally common, but the primary type is always linked to renal artery stenosis. 

Primary hypertension has no specific cause and accounts for more than 95% of cases, while secondary hypertension is due to another disease and constitutes 2-5% of cases. 

Primary hypertension constitutes 2-5% of cases and usually resolves with treatment of an underlying disorder, while secondary hypertension has no identifiable cause. 

Primary hypertension is caused by pheochromocytoma, while secondary hypertension is environmental.

Secondary hypertension is idiopathic and more prevalent in black individuals than primary. 

Non-selective β-blockers, due to their strong reduction in cardiac output.

ACE inhibitors, as they have reno-protective effects and minimal impact on glucose metabolism.

α₁-blockers, to avoid bronchospasm in asthma.

Loop diuretics, to manage hyperlipidemia.

Diuretics, for their efficacy in elderly black patients.

Mechanism: Decreases heart rate, force of contraction, and renin release; Adverse effect: Rebound hypertension upon sudden withdrawal.

Mechanism: Inhibits ACE to reduce bradykinin breakdown; Adverse effect: Hyperkalemia.

Mechanism: Selective β₁ blockade only; Adverse effect: Preferred in pregnancy-induced hypertension.

Mechanism: Vasodilation via α₁ blockade; Adverse effect: Ototoxicity.

Mechanism: Increases renin release; Adverse effect: Masks hypoglycemic symptoms in diabetics.

Cushing syndrome.

Middle-aged, 40 – 60 years old.

Pheochromocytoma.

Conn’s syndrome.

Hyperthyroidism.

It stimulates baroreceptors in the carotid arch to decrease sympathetic outflow.

It inhibits renin production in the kidneys in response to high intrarenal blood pressure.

It increases parasympathetic output to the heart, decreasing cardiac output.

It acts as a potent vasoconstrictor and promotes aldosterone release, leading to sodium retention and increased blood volume.

It blocks AT₁ receptors to cause vasodilation and reduce peripheral vascular resistance.

They can cause hyperuricemia and hypokalemia.

They may cause ototoxicity.

They have high efficacy and block 25% of Na⁺ reabsorption.

They are more effective than loop diuretics.

They decrease serum cholesterol levels.

ARBs.

Beta-blockers.

Calcium channel blockers.

Alpha-blockers.

ACE inhibitors.

Baroreceptors reset to a higher level, sustaining elevated BP.

Parasympathetic output increases, causing vasodilation.

Baroreceptors reset to a lower level, normalizing BP.

Renin release is inhibited, reducing aldosterone.

Cardiac output decreases independently of sympathetic activity.

Hyperkalemia and angioedema.

Dizziness, irregular heartbeat, nausea, vomiting, fainting, low blood pressure, and fatigue.

Blue vision and optic neuropathy.

Ototoxicity and hypercholesterolemia.

Parkinsonism and increased gastric acid secretion.