Adrenoceptors, Calcium, and Vasoconstriction in Normal and Hypertensive Humans

Fr, Bühler; Bolli, Peter; Erné, Paul; Kiowski, Wolfgang; Fb, Müller; Ul, Hulthén; Bh, Ji

doi:10.1097/00005344-198500076-00022

Cited by 15 publications

(5 citation statements)

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“…Because stimulation of platelet a2-adrenoceptors raises free cytosolic calcium, a fall in circulating catecholamines might have contributed to the observed decreases in platelet calcium by reducing the stimulation of these receptors. 24 The statistically significant reduction in heart rate and the tendency for plasma renin activity to fall despite decreased sodium intake provide further evidence for an attenuation of adrenergic tone during weight loss.…”

Section: Total Cholesterolmentioning

confidence: 94%

Effect of weight reduction in moderately overweight patients on recorded ambulatory blood pressure and free cytosolic platelet calcium.

et al. 1991

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T here exists a strong association between the prevalence of obesity and that of hypertension.1,2 There is increasing evidence that in obese patients weight loss induced by hypocaloric diet is associated with a fall in blood pressure,3'4 although this does not reflect the experience of all investigators.5 The results of trials dealing with changes in body weight and in blood pressure remain difficult to interpret. This is mostly because a real placebo phase corresponding to the period of weight loss cannot be planned for obvious reasons. The use of ambulatory blood pressure monitoring provides an opportunity to circumvent this problem, because in contrast to the blood pressure measured by the physician in his office, blood pressure recorded in the

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Section: Total Cholesterolmentioning

confidence: 94%

Effect of weight reduction in moderately overweight patients on recorded ambulatory blood pressure and free cytosolic platelet calcium.

et al. 1991

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“…A dose-dependent and enhanced calcium influx antagonistic vasodilator response was found in hypertensive patients for different calcium antagonists, such as for the dihydropyridine calcium antagonists, nifedipine, nitrendipine and nicardipine, as well as for the non-dihydropyridine calcium antagonist, verapamil' 28 ' in agreement with those found by Robinson et al} 21 \ The magnitude of vasodilation by the different calcium antagonists was comparable when applied at a maximal locally effective concentration avoiding systemic effects' 28 '. Comparison with other compounds showed that calcium influx-dependent vasodilation following calcium antagonists is similar to the vasodilatory response to post-ischaemic reperfusion and is about four times greater than that occurring in response to alpha-1 or alpha-2 blockade, and three times greater than the response to sodium nitroprusside' 29 '. There are a number of reports that calcium antagonists act by calcium influx inhibition as well as by interactions with the calcium pool and calcium extrusion from the cell' 1 -3 " 5 -7 '.…”

Section: Enhanced Calcium Influx-dependent Vasoconstriction In Esssenmentioning

confidence: 89%

Calcium antagonist induced vasodilation in peripheral, coronary and cerebral vasculature as important factors in the treatment of elderly hypertensives

Erné¹,

Conen²,

Kiowski³

et al. 1987

European Heart Journal

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Increased arteriolar tone is the pathophysiological hallmark of essential hypertension and is determined by the intracellular free calcium concentration in the vascular smooth muscle cell. Calcium influx is an important determinant of vasoconstriction and excess calcium influx-dependent vasoconstriction has been shown by plethysmographical studies in patients with essential hypertension. Calcium antagonists acutely lower BP by reducing calcium influx, calcium concentration and peripheral resistance. The degree of the attendant sympathetic nerve reflex activation and counter-regulatory mechanisms determines the antihypertensive response of the individual. Chronic monotherapy with a calcium antagonist results in an antihypertensive response, which is directly related to the patient's age and pretreatment BP and indirectly related to plasma renin levels. The resulting reduction in after-load neither leads to reduced cerebral blood flow in hypertensive patients, nor aggravates congestive heart failure. Calcium antagonists are a useful alternative to diuretics, primarily in older patients with low renin levels, either alone or combined with any other antihypertensive drug, and provide effective and safe control of blood pressure.

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“…The actions of adrenoceptors either at α - or β -receptors are mediated through G-protein-coupled receptors (GPCR) which in turn increases the intracellular calcium level via Ca 2+ channels. [11] Angiotensin-II, another potent vasoconstrictor, also activates GPCR stimulating PIP 3 -mediated pathway for the opening of L-type of Ca 2+ channels. [121314] Increased intracellular Ca 2+ in turn increases arteriolar muscle tone and also activates TRPV1 receptors.…”

Section: Introductionmentioning

confidence: 99%

A study to investigate capsaicin-induced pressure response in vagotomized rats

2013

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Objectives:Capsaicin is used to evoke pulmonary C reflexes and produces complex pressure responses along with apnea/tachypnea, and bradycardia. In the present study, the mechanisms involved in capsaicin-induced pressure responses were explored.Materials and Methods:Tracheal, jugular venous, and femoral artery cannulations were performed in anesthetized adult rats. Blood pressure, respiratory excursions, and electrocardiogram were recorded. Cardiorespiratory reflex changes evoked by jugular venous injection of capsaicin (10 μg/kg) were recorded in vagotomized and antagonist pretreated animals.Results:Capsaicin produced triphasic pressure response exhibiting immediate hypotension, intermediate recovery, and delayed hypotension. Time-matched respiratory changes showed apnea, bradypnea, and tachypnea, respectively. Bradycardia occurred at immediate and intermediate phases. After vagotomy, immediate hypotension was abolished; the intermediate recovery was potentiated as hypertensive response; and the delayed hypotension persisted. In case of respiration, the immediate bradypnea persisted and delayed tachypnea was abolished; while heart rate changes at immediate and intermediate phases were abolished. Antagonists of α1-adrenoceptor (prazosin or terazosin, 0.5 mg/kg), β-adrenoceptor (propranolol, 1 mg/kg), AT1 receptor (losartan, 10 mg/kg) and Ca2+ channel (diltiazem, 1 mg/kg) failed to block the capsaicin-induced intermediate hypertensive response in vagotomized animals.Conclusions:These observations implicate the existence of mechanisms other than adrenergic, angiotensinergic, or Ca2+ channel-dependent mechanisms for mediating the capsaicin-induced intermediate hypertensive response in vagotomized animals.

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Adrenoceptors, Calcium, and Vasoconstriction in Normal and Hypertensive Humans

Cited by 15 publications

References 0 publications

Effect of weight reduction in moderately overweight patients on recorded ambulatory blood pressure and free cytosolic platelet calcium.

Effect of weight reduction in moderately overweight patients on recorded ambulatory blood pressure and free cytosolic platelet calcium.

Calcium antagonist induced vasodilation in peripheral, coronary and cerebral vasculature as important factors in the treatment of elderly hypertensives

A study to investigate capsaicin-induced pressure response in vagotomized rats

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