The nurse preparing to administer both a calcium channel blocker and a beta1-adrenergic blocker to a client with hypertension plans to monitor the client's response based on which understanding of these drugs?
1. They promote calcium influx into vascular smooth muscle.
2. They block sympathetic impulses in sarcolemma membranes.
3. They prevent calcium influx into vascular smooth muscle.
4. They promote urinary excretion of sodium.
Correct Answer: 3
Rationale 1: Opening of calcium channels increases intracellular calcium and vascular smooth muscle contraction, raising blood pressure.
Rationale 2: Beta1-adrenergic blockers prevent sympathetic impulse generation that leads to calcium channel opening, but calcium channel blockers work at the level of the calcium ion channel, and do not directly suppress sympathetic impulse generation.
Rationale 3: Beta1-adrenergic blockers cause calcium ion channels to close by preventing sympathetic stimulation of membrane depolarization, and calcium channel blockers cause a change in calcium channel shape that prevents calcium influx into smooth muscle cells. Both mechanisms of drug action decrease intracellular calcium and prevent vascular smooth muscle contraction.
Rationale 4: Neither calcium channel blockers nor beta1-adrenergic blockers affect the renin-angiotensin-aldosterone system to promote urinary sodium excretion.
Global Rationale: Beta1-adrenergic blockers cause calcium ion channels to close by preventing sympathetic stimulation of membrane depolarization, and calcium channel blockers cause a change in calcium channel shape that prevents calcium influx into smooth muscle cells. Both mechanisms of drug action decrease intracellular calcium and prevent vascular smooth muscle contraction. Opening of calcium channels increases intracellular calcium and vascular smooth muscle contraction, raising blood pressure. Beta1-adrenergic blockers prevent sympathetic impulse generation that leads to calcium channel opening, but calcium channel blockers work at the level of the calcium ion channel, and do not directly suppress sympathetic impulse generation. Neither calcium channel blockers nor beta1-adrenergic blockers affect the renin-angiotensin-aldosterone system to promote urinary sodium excretion.
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