Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension.

Veld, A. J. Man In 'T; Wenting, G. J.; Boomsma, Frans; Verhoeven, R. P.; Schalekamp, M. A. D. H.

doi:10.1111/j.1365-2125.1980.tb01079.x

Cited by 28 publications

(5 citation statements)

References 14 publications

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“…Since heart rate changes associated with brief baroreflex stimulation probably result virtually entirely from changes in vagal outflow, [18][19] the results also are consistent with coexistent decreased vagal responsiveness and increased sympathetic activity in these patients. 20 The key issue in interpreting this reciprocal relationship is that of causality: If decreased baroreflex sensitivity and increased sympathetic outflow occur together in some individuals, which causes which, or does a third factor produce both?…”

Section: Discussionsupporting

confidence: 71%

Arterial baroreflex sensitivity, plasma catecholamines, and pressor responsiveness in essential hypertension.

Goldstein¹

1983

Circulation

133

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Arterial baroreflex sensitivity, plasma norepinephrine (NE) and epinephrine (E), and pressor and depressor responses were assessed in 25 patients with essential hypertension and 29 normotensive control subjects. Sensitivity of the cardiac limb of the baroreflex was determined by blood pressure and interbeat interval responses associated with the Valsalva maneuver, externally applied neck suction and pressure, and injection of phenylephrine and nitroglycerin. By all these techniques, patients with essential hypertension had significantly decreased baroreflex sensitivity, even after adjustment for age mismatching between the hypertensive and normotensive groups. Hypertensive patients also had significantly higher mean levels of plasma NE and E in both brachial arterial and antecubital venous blood (246 vs 154 pg/ml arterial NE, 286 vs 184 pg/ml venous NE, 99 vs 55 pg/ml arterial E, and 65 vs 35 pg/ml venous E) and significantly larger pressor responses to injected phenylephrine (30.9 mm Hg/100 ,)g vs 16.7 mm Hg/100 ,ug). When baroreflex-cardiac sensitivity values measured by the various techniques were averaged, there was a significant inverse relationship between sensitivity and venous NE and between sensitivity and pressor responsiveness. The results indicate that decreased baroreflex-cardiac sensitivity, increased sympathetic outflow, and pressor hyperresponsiveness tend to occur together in some patients with essential hypertension. Decreased arterial distensibility and altered central neural integration can account for these findings.Circulation 68, No. 2, 234-240, 1983. THE ARTERIAL baroreceptor reflex system constitutes one of the most powerful and rapidly acting homeostatic mechanisms for controlling blood pressure, and as such has attracted the interest of hypertension researchers for many years. Baroreflex sensitivity measured by the change in interbeat interval per unit change in systolic pressure after injection of a vasoconstrictor and after the Valsalva maneuver is significantly decreased in patients with essential hypertension. [1][2][3][4][5][6] However, in investigations in which externally applied neck suction has been used to increase carotid transmural pressure and thereby stimulate carotid baroreceptors, decreased baroreflex sensitivity in hypertension has not consistently been detected.7-9When directly compared, results obtained with these techniques have not agreed very well,'0 most likely because the techniques measure different aspects of baroreflex function. In this study, several different measurement techniques were used in each subject to determine if-and with what consistency across techniques patients with essential hypertension have decreased arterial baroreflex sensitivity. It was reasoned that averaging baroreflex sensitivities measured by all or several of the techniques might provide a more valid index of arterial baroreflex gain than relying on one technique alone.When baroreceptor afferents are stimulated, their reflexive circulatory effects result from vagal stimulat...

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Section: Discussionsupporting

confidence: 71%

Arterial baroreflex sensitivity, plasma catecholamines, and pressor responsiveness in essential hypertension.

Goldstein¹

1983

Circulation

133

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“…By contrast, the hemodynamic effects of altered autonomic control of heart rate and contractility may be relatively minor, since combined pretreatment with atropine and propranolol does not potentiate the vasodepressor response of supine hypertensive patients to intravenous bolus doses of diazoxide. 12 In conclusion, we have demonstrated associations between the degree of vasodepressor response seen with graded infusions of NP and both the baroreflex sensitivity and baseline blood pressure. The latter association possibly reflects structural vascular changes related to the degree of hypertension.…”

Section: Discussionmentioning

confidence: 57%

“…39 The dependence of the slope of the dose-response curve on the degree of tachycardia induced, rather than on the degree of sympathetic stimulation, may be because mechanisms other than sympathetic stimulation will contribute to the homeostatic response seen. Man in'T Veld et al 12 have shown that reduction of vagal tone is the principal mechanism for increase in HR and cardiac output seen when blood pressure is decreased with diazoxide. The degree of sympathetic stimulation will determine the reflexly mediated peripheral vasoconstriction that will oppose the vasodepression induced by NP.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex sensitivity modulates vasodepressor response to nitroprusside.

Shepherd¹,

Lin

McNay

et al. 1983

Hypertension

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SUMMARY Baroreflex activity is a determinant of the homeostatic response to alteration in blood pressure. We examined the factors that determine the magnitude of the vasodepressor response to sequential incremental intravenous infusions of sodium nitroprusside (NP), 0.05 to 6.4 yug/kg/min, in eight male patients with essential hypertension. Each infusion level was of 10 minutes' duration. Change from control values of mean arterial pressure (AMAP), heart rate (AHR) and plasma norepinephrine (ANE) were obtained at the end of each infusion level. Significant correlations were found between AMAP vs log dose NP, AHR vs AMAP and ANE vs AMAP for each patient (p < 0.05). However, the slopes of these relationships varied widely between subjects and were significantly correlated with the control blood pressure of each patient. In addition, the sympathetic responsiveness, as measured by ANE vs AMAP, was inversely correlated with the degree of vasodepressor response seen. Thus, the magnitude of the vasodepressor response was determined by two major factors: 1) the predrug blood pressure, possibly reflecting altered vascular geometry with hypertension; 2) the degree of sympathetic response, which probably acts by mediating the degree of reflex alpha-adrenergic-mediated arteriolar vasoconstriction. (Hypertension 5: 79-85, 1983) KEY WORDS * plasma norepinephrine • hypertension • heart rate • humans T HE level of baroreceptor activity, acting by way of the sympathetic nervous system, is a major determinant of the homeostatic response to perturbation of blood pressure. Changes in sensitivity of the baroreflex arc occur in hypertension, 1 " 5 sleep, 6 and with aging. Baroreflex sensitivity (BRS) is usually expressed in terms of the change in heart rate (HR), or R-R interval, for each unit of change in blood pressure.' 2 7~9 However, there are practical and theoretical limitations to this approach. First, in subjects receiving beta-adrenoceptor antagonists, the relationship between HR response and the level of sympathetic activity may change. Second, HR is controlled by a balance between the level of activity of the vagal and the sympa-

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“…21 The fall in arterial pressure was associated with increments in heart rate and cardiac output, probably by baroreflex-mediated withdrawal of vagal tone and increase in sympathetic activity. 22 The increased sympathetic activity was reflected by a rise in plasma norepinephrine. Despite continued sympathetic stimulation, cardiac output returned to its initial level.…”

Section: Discussion Cardiovascular and Hormonal Effects Of Ketanserinmentioning

confidence: 99%

5-HT, alpha-adrenoceptors, and blood pressure. Effects of ketanserin in essential hypertension and autonomic insufficiency.

Wenting¹,

Woittiez²,

Veld³

et al. 1984

Hypertension

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SUMMARY The serotonin (5-hydroxytryptamine, 5-HT) antagonist, ketanserin, has a high affinity for 5-HT 2 -receptors but it also binds to a^adrenoceptors. The compound (10 mg i.v.) lowered mean arterial pressure by 22% ± 2% (mean ± SEM, p < 0.001) in 30 patients with essential hypertension. Measurements of heart rate, cardiac output, cardiac filling pressures, forearm blood flow, renal blood flow, and glomerular filtration rate revealed a hemodynamic pattern compatible with vasodilation of both resistance and capacitance vessels. This was accompanied by moderate reflex cardiostimulation. Ketanserin did not alter the pressor effect of bolus injections of (-)-phenylephrine hydrochloride ( A LTHOUGH 5-hydroxytryptamine (5-HT, serotonin) was among the first vasoactive amines . to be discovered and synthesized, its function in blood pressure regulation is still unclear. Recently, a differentiation between two subtypes of 5-HT-receptors has been made on the basis of radioligand-binding studies using membranes prepared from rat frontal cortex.1 Although specific functions associated with these brain receptors have not been identified, it has been shown that the 5-HT-receptors subserving contraction of vascular smooth muscle cells are of the 5-HT 2 -subtype. for clinical investigation. 4 " 6 Ketanserin, however, is not fully specific for 5-HT 2 -receptors, since it also binds to a,-adrenoceptors. High concentrations of ketanserin have an antagonistic effect on a,-adrenoceptor-mediated contractions of isolated arteries and veins. 4 Experiments in animals 4 and preliminary data in humans 8 9 have shown that ketanserin has antihypertensive properties. This may, at least in part, depend on blockade of a,-adrenoceptors. Indeed, it has been reported that hypotensive doses of ketanserin abolished the pressor response to a,-agonists in the pithed rat, the anesthetized normotensive rat, and the conscious spontaneously hypertensive rat.10 " This paper describes the hemodynamic profile of ketanserin's antihypertensive action in patients with essential hypertension. The possibility that the antihypertensive effect of ketanserin depends on interference with a,-adrenoceptor-mediated vasoconstriction was tested by comparison of the pressor effects of the a,-adrenoceptor agonist, phenylephrine, before and after ketanserin and by assessment of the antihypertensive effect of ketanserin after administration of the a,-adre-

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Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension.

Cited by 28 publications

References 14 publications

Arterial baroreflex sensitivity, plasma catecholamines, and pressor responsiveness in essential hypertension.

Arterial baroreflex sensitivity, plasma catecholamines, and pressor responsiveness in essential hypertension.

Baroreflex sensitivity modulates vasodepressor response to nitroprusside.

5-HT, alpha-adrenoceptors, and blood pressure. Effects of ketanserin in essential hypertension and autonomic insufficiency.

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