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Biomedical subjects

W Kiowski

Publications and source records attributed to W Kiowski.

At least 181 records · Page 10Linked to original sources
PubMed1983

Verapamil-induced vasodilator response is enhanced in essential hypertension.

Forearm blood flow response to the calcium channel inhibitor verapamil, 1 75 micrograms/100 ml tissue, as measured by venous occlusion plethysmography, was found to be significantly greater in 11 patients with essential hypertension as compared to 11 age-matched normotensive subjects whereas there was no significant difference in increase in forearm blood flow between both groups to non-specific vasodilatation with sodium nitroprusside (1.2 micrograms/100 ml tissue). The increase in forearm blood flow to verapamil correlated positively with basal plasma epinephrine concentration in hypertensives. These findings support the concept of an increased dependency of arteriolar tone on calcium influx in patients with essential hypertension, an abnormally related to the activity of the sympathetic nervous system.

Adult↗
PubMed1983

Inhibition of the arteriolar smooth muscle NA+ -K+-pump induces an enhanced vasoconstriction in borderline but not in established essential hypertension.

1. The dependency of arteriolar tone on the activity of the Na+ -K+-pump was studied in 17 normotensive (NT) males, aged 20-71 yr, without heredity for essential hypertension and 28 male patients with essential hypertension, aged 18-63 yr, by measuring forearm blood flow response to intra-arterial infusion of the Na+-K+-pump inhibitor ouabain. 14 of the patients were classified as borderline essential hypertensives (BHT) and 14 as established essential hypertensives (EHT). 2. Ouabain in incremental dosages 0.4-16 micrograms/100 ml tissue induced a vasoconstrictive response in the forearm with a maximal effect to 8 micrograms/100 ml tissue, which was not associated with an increase in regional noradrenaline release. 3. The vasoconstriction to ouabain 8 micrograms/100 ml was 29.6 +/- 6.8% in NT (P less than 0.001); 51.9 +/- 8.4% in BHT (P less than 0.001) and 36.0 +/- 12.7% in EHT (P less than 0.05). This response was greater in BHT than in NT (P less than 0.05) but not different in NT and EHT and did not correlate with age either in NT or in BHT and EHT taken together. 4. Our findings suggest an increased activity of the arteriolar Na+ -K+-pump in the early phase of essential hypertension which may to some extent correct a raised intracellular Na+; the latter being the consequence of an increased passive permeability to Na+. The activity of the arteriolar Na+ -K+-pump appears to be decreased in the later as compared to the early phase of essential hypertension.

Adolescent↗
PubMed1983

Alpha 2 adrenoceptor-mediated vasoconstriction of arteries.

We investigated the possibility that adrenoceptors of the alpha 2 subtype mediate vasoconstriction of arteries in response to administered catecholamines. Clonidine, which in vitro, stimulates alpha 2-adrenoceptors was infused into a brachial artery in 12 subjects (0.48 micrograms/min/100 ml tissue for 3 min). Afterward, prazosin was infused intraarterially in the first six subjects (0.5 micrograms/min/100 ml for 10 min) and in the remaining subjects, phentolamine was infused (0.12 micrograms/min/100 ml) for 10 min. Subsequently, the clonidine infusion was repeated. Clonidine decreased forearm blood flow from 3.5 +/- 0.52 to 1.8 +/- 0.32 in the first six subjects and from 4.2 +/- 0.84 to 2.7 +/- 0.61 ml/min/100 ml in the other subjects. Alpha 1-Adrenoceptor blockade by prazosin increased forearm blood flow by 122.7 +/- 33.8% and combined alpha 1 and alpha 2 blockade by phentolamine by 127.2 +/- 29.9%, indicating much the same degree of postjunctional alpha-adrenoceptor blockade. Alpha 2-Adrenoceptor-mediated vasoconstriction by clonidine was abolished after phentolamine (9.1 +/- 2.29 and 9 +/- 2.51 ml/min/100 ml) but was still present after prazosin (7.8 +/- 1.7 and 4.8 +/- 1.6 ml/min/100 ml). The results suggest that, apart from the classical alpha 1 adrenoceptor, there is a second type of adrenergic receptor on smooth muscle cells that can mediate vasoconstriction, resembling the alpha 2-adrenoceptor pharmacologically.

Adult↗
PubMed1983

Alpha-adrenoceptors, adrenaline, and exaggerated vasoconstrictor response to stress in essential hypertension.

Stressful sympathetic stimulation by cold pressor test in patients with essential hypertension results in an exaggerated response of the already elevated plasma adrenaline, heart rate, blood pressure, and alpha-adrenoceptor-mediated vasoconstriction when compared with normotensive subjects. The stress-induced increase in adrenaline was correlated with the attendant increase in blood pressure. The stress-induced reduction in forearm flow was reversed during infusion of the postjunctional alpha 1-adrenoceptor blocker prazosin. Therefore, enhanced responses to sympathetic stress, as reflected and perhaps caused by an exaggerated rise in plasma adrenaline, may contribute to an increased alpha 1-adrenoceptor-mediated vasoconstriction in essential hypertension.

Adult↗
PubMed1983

Cardiopulmonary mechanoreceptors and renin release in humans.

We investigated the hemodynamic determinants of the reflex release of renin to changes in posture and blood volume distribution in healthy humans to determine the relative contribution of arterial and cardiopulmonary mechanoreceptors to the reflex release of renin under physiological circumstances. In the first experiments, we induced a selective decrease of right atrial pressure by inflation of cuffs around the thighs. Renin increased and returned toward baseline on decompression. The renin increase was neurogenic because plasma norepinephrine increased, the response was abolished by beta blockade, and renin did not increase in patients with denervated transplanted kidneys. The second experiments were performed with tilting and later filling a pressure suit to counteract the effect of tilting on gravitational pooling of the blood. Tilting elicited increases of renin and norepinephrine; filling the suit abolished these increases. Right atrial pressure fell with tilting and rose after filling the suit. Because the neck was elevated above the heart equally in both conditions, it is concluded that the increase and decrease of renin reflected decrease and increase of the stretch of cardiopulmonary receptors. The third experiments were performed by elevating the upper trunk with the legs remaining in a horizontal position (sitting). This caused a heart-to-neck pressure difference and an increased sympathetic outflow through unloading arterial baroreceptors. Norepinephrine increased but renin did not. Cardiopulmonary receptors exhibit an important influence on the reflex release of renin.

Blood Pressure↗
PubMed1982

Simplified antihypertensive therapy with pindolol retard.

36 out of 52 patients with essential hypertension, whose blood pressure was not normalized with pindolol 15 mg per day, were treated with 30 mg per day for four to six weeks. Pindolol was administered in random order, either as 15 mg twice daily or as one 30 mg retard tablet once daily. Blood pressure was lowered from mean pretreatment levels of 174/111 mmHg to 149/98 mmHg by 15 mg b.d., and to 145/97 mmHg by 30 mg retard. In five patients diurnal variations in blood pressure and plasma pindolol levels were determined. At all times during the day blood pressure was at least well controlled by 30 mg retard as by 15 mg b.d. Plasma concentration maxima were similar with both forms, but a higher concentration was maintained for a longer time after the retard tablet. Pindolol 30 mg was well tolerated and the incidence of side effects was lower than during treatment with 15 mg b.d. Thus, patients requiring high doses of pindolol for control of hypertension can safely and conveniently be treated with a single tablet of 30 mg pindolol retard.

Blood Pressure↗
PubMed1982

Antihypertensive and renal effects of captopril in relation to renin activity and bradykinin-induced vasodilation.

The effect of captopril on blood pressure and renal hemodynamics in relation to plasma renin activity (PRA) was assessed together with the vasodilator responses to brachial artery infusions of bradykinin (BK) and sodium nitroprusside (NP) before and after 4 wk of therapy with doses of up to 450 mg/day in patients with essential hypertension. The average blood pressure reduction of captopril was from 174.4/110.6 to 155.3/96.6 mm Hg (n = 12, P less than 0.001) without increases in heart rate or body weight. It was effective in the eight patients with normal renin, but showed little effect in the four with a low renin. There was a correlation between the changes in blood pressure after captopril and the pretreatment PRA (r = -0.82, P less than 0.01 for mean pressure). Brachial artery infusions of BK and NP induced dose-dependent rises in forearm blood flow (FBF), but this was not related to the captopril blood pressure-lowering effect. Repeat measurements during captopril therapy showed a shift to the left of the BK/FBF, but not of the NP/FBF, dose-response curve, indicating effective vascular kininase II inhibition. Captopril decreased renal vascular resistance. Our data are compatible with the view that captopril's antihypertensive action mainly involves blockade of the renin-angiotensin-aldosterone system and not cumulation of BK. The favorable effects on renal hemodynamics and the lack of tachycardia and volume retention after captopril make it a valuable drug for the treatment of hypertension.

Adult↗
PubMed1982

Elevated adrenaline and increased alpha-adrenoceptor-mediated vasoconstriction in essential hypertension.

In patients with essential hypertension, plasma adrenaline, regardless of age, was consistently higher than in normotensive controls; adrenaline correlated with heart rate and the vasodilator response in the forearm circulation produced by postjunctional alpha 1-adrenoceptor blockade with prazosin. This dilator response to prazosin was greater in hypertensive patients. Together, this suggests elevated sympathetic activity and enforced vasoconstriction via postjunctional alpha 1-adrenoceptors in essential hypertension. beta-Adrenoceptor-mediated cardiovascular responses decrease with age and even more with high blood pressure, which contributes to unopposed alpha-adrenoceptor-mediated vasoconstriction. This could explain the transition from an early high cardiac output into a later high peripheral resistance form of hypertension.

Adaptation, Physiological↗
PubMed1982

Verapamil-induced vasodilation is enhanced in essential hypertension.

The dependency of arteriolar tone on calcium influx was studied in 11 patients with essential hypertension (EHT) and compared to 11 age-matched normotensive (NT) subjects by measuring the forearm blood flow (FAF) response to intraarterial infusion of the calcium channel blocker verapamil (Verap) and the nonspecific vasodilator sodium nitroprusside (Nip) with venous occlusion plethysmography. Verap in incremental dosages induced a greater increase in forearm blood flow (delta FAF) in EHTs than in NTs, whereas there was no significant difference in delta FAF following Nip. When delta FAF to Verap was adjusted for delta FAF to Nip, it was still greater in EHTs. In EHTs delta FAF to all dosages of Verap correlated positively with basal plasma epinephrine concentration, and at the two highest dosages of Verap, associated with a decrease in systemic blood pressure, it correlated negatively with plasma renin activity and plasma angiotensin II concentration. Thus, increased dependency of arteriolar tone on calcium influx is related to the activity of the sympathetic nervous system in EHT. This association may be due to a common derangement in transmembranous ionic fluxes in the vascular smooth muscle cells and sympathetic neurons in EHT.

Adult↗
PubMed1982

The place of the calcium antagonist verapamil in antihypertensive therapy.

The antihypertensive efficacy of the calcium antagonist verapamil was tested in 43 patients with essential hypertension, examining relationships between age and pretreatment renin and blood pressure and comparing intraindividually the responses with those obtained using beta-blockers (n = 29) and diuretic therapy (n = 18). Verapamil produced a decrease in mean blood pressure that was directly related to the patient's age and pretreatment blood pressure but inversely to pretreatment renin. Although there was no difference in overall pressure response between verapamil, beta-blocker, and diuretic therapy, the pressure responses with diuretics paralleled those obtained with verapamil, whereas, in contrast, responses with beta-blockers correlated indirectly with the patient's age and directly with pretreatment renin. These data provide the basis for a new antihypertensive treatment concept proposing a calcium antagonist as the first choice for the older and low renin patients in place of a diuretic agent and a beta-blocker as the first-line drug for the younger and high renin patients.

Adrenergic beta-Antagonists↗
PubMed1981

Reliability of echocardiography in assessing cardiac output. A comparative study with a dye dilution technique.

Because of the potential benefits froma noninvasive technique in assessing cardiac output, we compared cardiac output estimates from left ventricular echocardiograms with results obtained simultaneously by a standard technique, dye dilution in 10 healthy normal volunteers. During rest, cardiac outputs by echocardiographic and dye dilution techniques were reproducible and not significantly different. Increases in cardiac output produced by intravenous infusion of isoproterenol (15 ng/kg/min for 4 min) were accurately estimated by echocardiography in subjects whose stroke volume increased less than 40%, but were significantly underestimated when stroke volume increased more than 40%. Decreased cardiac output produced by intravenous propranolol (0.2 mg/kg) was comparable by both methods. Although echocardiography accurately estimated mean cardiac output for the group it over- or underestimated cardiac output in individual subjects. We propose that echocardiography can reliably estimate cardiac output in groups at rest and when stroke volume changes less than 40%.

Cardiac Output↗
PubMed1981

Plasma noradrenaline concentration and alpha-adrenoceptor-mediated vasoconstriction in normotensive and hypertensive man.

1. Plasma noradrenaline concentrations and blood pressure were measured in 45 patients with essential hypertension and 34 matched normotensive subjects. Plasma noradrenaline was similar in both groups, but in the hypertensive patients plasma noradrenaline correlated with blood pressure. 2. The increase in forearm flow in response to an intra-arterial infusion of phentolamine was determined in 12 of the hypertensive and 14 of the normotensive subjects to assess the alpha-adrenoceptor-mediated component of vascular resistance. Although the dilator response to phentolamine was similar in both groups, in the hypertensive patients it was correlated with the control plasma noradrenaline (r = 0.83, P less than 0.01) as well as the height of mean blood pressure (r = 0.73, P less than 0.01). 3. These results suggest that in hypertensive patients plasma noradrenaline can be a marker for both sympathetic activity and the alpha-adrenoceptor-mediated component of vascular resistance.

Adolescent↗
PubMed1981

Age-related decrease in cardiac and peripheral vascular responsiveness to isoprenaline: studies in normal subjects.

1. Changes in forearm blood flow to intra-arterial infusion of isoprenaline and the chronotropic response to intravenous boluses of isoprenaline were measured in 15 healthy volunteer subjects, eight younger than 25 years and seven older than 50 years. Intra-arterial blood pressure and basal plasma renin activity, adrenaline and noradrenaline were also measured. 2. Young subjects exhibited a greater increase in forearm blood flow than old subjects, to all four doses of isoprenaline used, a greater cardiac isoprenaline responsiveness (measured by the increase in heart rate; P less than 0.001) and a higher renin (P less than 0.02). 3. Resting values of blood pressure, forearm blood flow, adrenaline and noradrenaline were not significantly different in young and old subjects. In the latter, noradrenaline correlated with forearm blood flow (r = -0.77, P less than 0.05), forearm vascular resistance (r = 0.86, P less than 0.02) and mean arterial pressure (r = 0.83, P less than 0.02), whereas in the younger subjects forearm blood flow was related to adrenaline (r = 0.78, P less than 0.05). 4. These data provide evidence for an age-related parallel reduction in cardiac, peripheral vascular and renal beta-adrenoceptor-mediated responses.

Adolescent↗
PubMed1980

[Enhanced alpha adrenoreceptor-mediated vasoconstrictor component in essential hypertension].

Changes in forearm blood flow in response to infusions of the postsynaptic alpha blocking agent prozosin (0.5 microgram/min/100 ml forearm tissue) and of the nonspecific vasodilating drug sodium nitroprusside (0.6 microgram/min/100 ml forearm tissue) into the brachial artery were assessed in 24 patients with essential hypertension (EHT) and in 16 age-matched normotensive subjects (NT). Under basal conditions forearm blood flow was higher in EHT (4.0 +/- 0,2 vs. 2.6 +/- 0.3 ml/min/100 ml forearm tissue, p less than 0.001). Forearm blood flow response to prazosin was greater in EHT than in NT (7.7 +/- 0.8 vs. 2.6 +/- 0.3, p less than 0.001) while sodium nitroprusside responses were similar in EHT and NT (13.8 +/- 0.8 vs 13.0 +/- 0.8 vs. 13.0 +/- 0.1, n.s.). These results indicate an enhanced alpha adrenoceptor-mediated vasoconstrictor component in EHT and help to explain the effectiveness of antihypertensive drugs which interfere with sympathetic control of vascular resistance.

Adult↗
PubMed1980

Plasma catecholamines and cardiac, renal and peripheral vascular adrenoceptor-mediated responses in different age groups of normal and hypertensive subjects.

The role of the sympathetic nervous system in cardiac, renal and peripheral vascular adrenoceptor-mediated responses was investigated in patients with essential hypertension and age-matched normotensive subjects. Regardless of age plasma adrenaline was significantly higher in hypertensive when compared with normotensive subjects. This suggests a sympatho-adrenal factor in essential hypertension. Plasma noradrenaline tended to increase with age but its similarity between normotensive and hypertensive subjects points to similar postganglionic neural activity and/or similar overflow of noradrenaline into the circulation. On the other hand, beta-adrenoceptor-mediated tachycardia in response to exercise and intravenous isoproterenol as well as the forearm vasodilator response to intraarterial isoproterenol decreased in normal subjects with older age. In hypertensives this age-dependent beta-receptor-related effect tends to be enhanced as judged from the greater reduction of cardiac isoproterenol sensitivity and the blunted renin response to exercise stimulation. The dilator response to alpha-adrenoceptor blockade with phentolamine was not different in both groups. Therefore a qualitative rather than quantitative derangement of sympathetic control of vascular resistance - in which beta-dilator effects are reduced and alpha-constrictor mechanisms prevail - may contribute to the maintenance of established hypertension.

Adult↗
PubMed1979

Plasma noradrenaline correlates with alpha-adrenoreceptor-mediated vasoconstriction and blood pressure in patients with essential hypertension.

1. The relationships between plasma noradrenaline concentration at rest and blood pressure, as well as increase in forearm blood flow in response to a brachial artery infusion of the alpha-adrenoreceptor-blocking agent phentolamine, were investigated in hypertensive and normotensive subjects of similar age. 2. In 44 hypertensive patients plasma noradrenaline correlated with systolic, diastolic and mean blood pressures, but no difference in the mean plasma noradrenaline concentration was found. 3. In 11 patients and 14 normotensive subjects alpha-adrenoreceptor blockade resulted in a similar increase in forearm blood flow. Only in the patients, however, was this increase related to plasma noradrenaline and blood pressure. 4. In patients with established essential hypertension plasma noradrenaline can be considered to be a marker of alpha-adrenoreceptor-mediated vasoconstriction, which, in part, determines the height of the blood pressure.

Adolescent↗