A 62-year-old man with hypertension initiated on nifedipine presents with flushing, headache, and bilateral ankle edema. Vital signs show BP 128/76 mmHg, HR 88 bpm, RR 16, temp 37°C, SpO2 98%. Echocardiography reveals normal ejection fraction and no evidence of heart failure. He denies orthopnea or dyspnea on exertion. Which of the following best explains nifedipine's predominant mechanism of action producing these adverse effects?
- A)Blockade of beta 1 receptors in the myocardium
- B)Venous dilation through nitric oxide donation
- C)Inhibition of angiotensin converting enzyme
- D)Arteriolar smooth muscle relaxation through L type calcium channel blockadeGABARITO
- E)Direct inhibition of renin release
Explicação
Dihydropyridine calcium channel blockers such as nifedipine act mainly on vascular smooth muscle, causing arteriolar vasodilation. Reflex tachycardia, flushing, headache, and peripheral edema are characteristic consequences of this mechanism. Ver explicação completa e trilha adaptativa →