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Increased cardiovascular responses to norepinephrine and calcium antagonists in essential hypertension compared with
Insights
Essential hypertension involves heightened responses to rest and norepinephrine (NE), contributing to elevated blood pressure. Calcium channel blockers effectively reduced NE effects, suggesting a role in managing hypertension.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Essential hypertension is characterized by elevated blood pressure without a clear secondary cause.
- Understanding the physiological responses to vasoactive substances is crucial for hypertension management.
Purpose of the Study:
- To investigate cardiovascular and vascular resistance responses to supine rest, norepinephrine (NE), and angiotensin II (Ang II) in essential hypertension versus normotension.
- To evaluate the effects of calcium antagonists (nifedipine, diltiazem) on these responses.
Main Methods:
- Human participants with essential hypertension and normotensive controls underwent physiological measurements.
- Responses to supine rest, NE, and Ang II were assessed with and without nifedipine or diltiazem administration.
Main Results:
- Supine rest decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI), but increased total peripheral vascular resistance index (TPRI).
- NE increased BP and TPRI, while decreasing HR, SI, and CI. These increases were more pronounced in hypertensives.
- Nifedipine and diltiazem inhibited NE-induced increases in BP and TPRI, but diltiazem did not inhibit Ang II-induced increases.
Conclusions:
- Early-stage essential hypertension exhibits heightened responses to rest and NE, potentially contributing to elevated BP.
- Calcium antagonists inhibit NE-dependent calcium influx/release in arterial smooth muscle.
- Ang II-induced responses suggest calcium antagonists may not affect Ang II-dependent calcium channel activity.
Abstract:
The responses to a supine rest, norepinephrine (NE) and angiotensin II (Ang II) were investigated in the absence and presence of calcium antagonist nifedipine or diltiazem in essential (genetic, arterial) hypertension and normotension in humans. A supine rest significantly decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI). On the contrary, the rest increased total peripheral vascular resistance index (TPRI) in both normotensives and hypertensives. The decrease in BP was significantly greater in hypertensives than in normotensives. NE significantly increased BP and TPRI, whereas it decreased HR, SI, and CI. The increase in BP was greater in hypertensives than in normotensives. Nifedipine and diltiazem inhibited the NE-induced increases in BP and TPRI. Ang II increased BP and TPRI, but it decreased HR, SI, and CI. Diltiazem did not inhibit the Ang-II-induced increases in both BP and TPRI. The increased responses to a rest and NE were observed in the early stage of essential hypertension. The increased responses may contribute to both the increase in BP and the induction of high blood pressure in essential hypertension. The calcium antagonists inhibited the NE-induced increases in BP and TPR. The results suggest that the antagonists inhibit the NE-dependent calcium influx and calcium release in the arterial smooth muscle. The observed responses to Ang II suggest that the antagonists may not inhibit Ang-II-dependent calcium-channel activity in the smooth muscle.