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Biomedical subjects

M L Muiesan

Publications and source records attributed to M L Muiesan.

105 records · Page 6Linked to original sources
PubMed1986

Renal noradrenergic and dopaminergic activity in patients with borderline essential hypertension.

An opposite modulatory influence of renal noradrenergic and dopaminergic activities on sodium excretion has been suggested. In this study urinary noradrenaline (UNA) and dopamine (UDA) excretion were evaluated in patients with borderline essential hypertension (BH; n = 9) and in patients with established essential hypertension (EH; n = 11) as well as in normal subjects (NT, n = 8), during normal sodium and potassium intake. Measurements were performed on fractionated urine collections on two separate days: on the first day under basal conditions and on the second day after saline infusion (SAL), 2L/2h, i.v. In BH, basal UNA and UDA were higher with respect to NT and EH. The difference was significant (p less than 0.05) in urine collected between 8 and 14 h. In all three groups, SAL induced a significant decrease in UNA and a significant increase in UDA; the decrease in UNA after SAL was significantly lower in EH in respect to BH and NT. In conclusion, the increased UDA in BH may represent a compensatory mechanism to a defect in sodium excretion, possibly due to elevated renal and/or systemic noradrenergic activity; the normal response to volume and salt loading suggests that the physiological modulation of sympathetic tone is still preserved in BH.

Adult↗
PubMed1985

Effect of pinacidil on blood pressure, plasma catecholamines and plasma renin activity in essential hypertension.

Pinacidil, a new cyanoguanidine derivative, is an antihypertensive agent with arteriolar vasodilating properties, which acts on precapillary resistance vessels. A trial was carried out in 30 patients with essential hypertension WHO I-II. The treatment period was divided into three phases. Hydrochlorothiazide (HCTZ) and amiloride were administered for 4 weeks in Phase 1 and supine and standing blood pressure decreased significantly. During Phase 2 pinacidil was added to HCTZ/amiloride for the following 3 months. A further significant reduction in blood pressure was obtained. In the next period of treatment (Phase 3) patients were divided into two groups. For 1 month Group A (15 patients) received pinacidil alone and Group B (15 patients) received HCTZ/amiloride. Conventional laboratory blood tests in all patients remained unchanged during treatment. Reported side effects during Phase 2 were headache (2 patients), dizziness (3 patients), palpitations (2 patients) and ankle oedema (2 patients). Plasma renin activity was slightly increased at the end both of Phases 1 and 2. Plasma catecholamines were increased but not significantly at the end of Phase 2 as compared to Phase 1. The results indicate that pinacidil is effective in lowering blood pressure in mild to moderate essential hypertension.

Adult↗
PubMed1985

Interrelations of cardiac and arterial vascular wall hypertrophy in essential hypertension.

Structural vascular changes in the calf arteries and left ventricular mass were measured in 52 essential hypertensive patients (WHO I and II, 35 men and 17 women, age range 21-63 years). Left ventricular mass was measured on M-mode echocardiographic tracings. Structural vascular changes were evaluated indirectly by studying the minimal vascular resistance, calculated from mean arterial pressure and maximal (post-ischaemic) blood flow, measured by venous occlusion plethysmography. A statistically significant correlation between left ventricular mass and minimal vascular resistance was observed (r = 0.33, P < 0.05). The low correlation suggested that structural changes in the heart and in the systemic arteries did not develop simultaneously. In the subgroup of patients with minimal vascular resistance in the normal range, left ventricular hypertrophy was found in 15 out of 30 patients (50% of cases) whereas, in the subgroup of patients with high minimal vascular resistance, absence of left ventricular hypertrophy was found in six out of 22 patients (27% of cases). These results suggest that left ventricular hypertrophy more often precedes arterial structural changes in the calves.

Adult↗
PubMed1985

Adrenergic activity and myocardial anatomy and function in essential hypertension.

In hypertension, changes of cardiac anatomy and function are not just a simple consequence of the increased pressure load. The sympathetic nervous system activity is one of the factors which may influence the cardiac performance, and possibly also the cardiac anatomy of hypertensive patients. Several clinical studies have provided evidence of a subset of patients, usually with mild or borderline hypertension, with an increased cardiac performance, higher plasma catecholamine concentrations and/or greater response to beta-adrenergic stimulation. Animal studies have strongly suggested a possible role of adrenergic factors in the development of left ventricular hypertrophy (LVH). In man, plasma catecholamines are usually higher in hypertensive patients with LVH, and a correlation between left ventricular mass and plasma noradrenaline has also been observed. An impaired response to beta-adrenergic stimulation has been reported in hypertensive animals and in patients with LVH. Several studies have also suggested that reversal of LVH may be more easily induced by those antihypertensive drugs that reduce, or at least do not stimulate, the sympathetic activity, although exceptions to this statement may be observed.

Animals↗
PubMed1984

Efficacy of low-dose captopril given twice daily to patients with essential hypertension uncontrolled by a beta blocker plus thiazide diuretic.

Thirty-two patients with moderate to severe essential hypertension whose supine diastolic blood pressure (SDBP) was greater than or equal to 95 mm Hg following 2 weeks' treatment with the optimal dosage of beta blocker-diuretic combination were randomly assigned to the addition of either captopril 25 mg or 50 mg b.i.d. After 6 weeks' treatment, if patients were not normalized (SDBP less than 95 mm Hg), the dose of captopril was doubled for a further 6 weeks. The addition of captopril led to a significant fall in standing and supine diastolic and systolic blood pressure at the end of the sixth and twelfth week of treatment. There was no difference in the change in blood pressure between the two groups. At the end of the study SDBP was normalized in 66% of patients and a further 12.5% had their SDBP reduced by greater than 10%. Captopril 25 or 50 mg administered twice daily proved to be a very effective antihypertensive agent when added to a beta blocker-diuretic combination in patients resistant to optimal doses of these drugs.

Adult↗
PubMed1982

The acute and chronic hypotensive effect of labetalol and the relationship with pretreatment plasma noradrenaline levels.

1 Labetalol 100 mg was given intravenously to 27 patients with essential hypertension (12 males, 15 females; WHO I-II; age range 30-66 yr; on average, a significant reduction of blood pressure was observed within 5 min (P less than 0.001). Average heart rate was also reduced significantly (P less than 0.01). 2 In 18 patients haemodynamic measurements were performed (dye-dilution or thermodilution technique): blood pressure reduction was related to peripheral vasodilatation, as cardiac index remained unmodified. 3 The absolute and percentage decrease of blood pressure, heart rate and total peripheral resistance after labetalol 100 mg intravenously, was significantly greater in the patients with higher baseline plasma noradrenaline concentration values. 4 In 12 out of 27 patients labetalol was given orally for 2 months (dose range 300-1200 mg); the pattern of blood pressure and heart rate changes after oral therapy were comparable to those observed after acute administration of the drug. 5 The degree of blood pressure and heart rate reductions after oral labetalol was also significantly related to pretreatment basal noradrenaline concentration.

Administration, Oral↗
PubMed1982

Adrenergic activity in systolic hypertension.

Basal hemodynamics and plasma catecholamines were measured in 10 patients with systolic hypertension, 7 males and 3 females, aged 38-69 years (Group 1), and in 10 patients with systolic and diastolic hypertension, 7 males and 3 females, aged 40-65 years (Group 2); the same measurements were repeated after acute pharmacological alpha and beta-blockade with Labetalol, 100 mg iv, or Propranolol, 10 mg iv, plus Phentolamine, 10 mg iv. In patients of Group 1 plasma noradrenaline was inversely related to systolic arterial pressure and to stroke index and was directly related to heart rate. In patients of Group 2 plasma noradrenaline was directly related to systolic arterial pressure. After acute alpha and beta-blockade the degree of reduction of systolic arterial pressure was directly related to basal plasma noradrenaline in both groups; systolic arterial pressure was reduced to normotensive levels in 5 patients of Group 1 who had high basal plasma noradrenaline values. These results confirm some of our previous findings and suggest that in some patients with systolic hypertension adrenergic activity is increased and may have a significant role in maintaining high blood pressure values.

Aged↗
PubMedDate not supplied

High-dose, not low-dose insulin increases the vasoconstrictor effect of norepinephrine in spontaneously hypertensive rats: effects of antihypertensive treatment.

The effect of insulin on the vasoconstriction induced by norepinephrine is presently controversial. Therefore, the aims of our study were: (1) to evaluate the effect of low- and high-dose insulin on the concentration-response curve to norepinephrine in small resistance arteries of spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) before and after the development of hypertension, and (2) to evaluate the effects of antihypertensive treatment on vascular response to insulin and norepinephrine. Fifty-six rats were included in the study. Six SHR were treated with enalapril and 6 with candesartan cilexetil from the 4th to the 12th week of age, while 10 WKY and 14 SHR were kept untreated. Two additional groups of 10 untreated SHR and 10 WKY were killed at 4 weeks of age, in a prehypertensive phase. Mesenteric small arteries were dissected and mounted on a micromyograph. A dose-response curve to norepinephrine was performed at cumulative concentrations in the presence or absence of low- and high-dose insulin. We found that only high-dose insulin increased the vascular response to norepinephrine in 12-week-old SHR, but not in 4-week-old SHR or in age-matched WKY. The increased responsiveness to norepinephrine disappeared after preincubation of the vessels with a selective inhibitor of endothelin-1 type A receptors. After antihypertensive treatment with enalapril or candesartan cilexetil, the potentiation of the vasoconstrictor response to norepinephrine was abolished. In conclusion, insulin at high, nonphysiological doses seems to induce an increase in the reactivity to norepinephrine in mesenteric small arteries of SHR, possibly mediated by a local production of endothelin-1. Antihypertensive treatment with an ACE inhibitor or an angiotensin II receptor blocker may normalize this altered response. This mechanism may be relevant in the development of hypertension in SHR.

Angiotensin Receptor Antagonists↗
PubMedDate not supplied

Cardiovascular structural alterations in hypertension: effect of treatment.

Available data support the hypothesis that antihypertensive drugs may determine a significant regression of cardiac and vascular structural changes. Antihypertensive drugs that inhibit the renin-angiotensin or, to a lesser extent, the adrenergic system may more consistently and promptly reduce left ventricular hypertrophy (LVH) and vascular structural changes. It is possible that all antihypertensive agents, when used for long enough periods, will reduce LV mass, whereas only certain drugs will reduce mass within a period of few months, so that any difference among classes of antihypertensive drugs is more quantitative than absolute. However, a rapid reversal of LVH may be particularly important because reducing blood pressure in the presence of an elevated LV mass may be associated with impairment of coronary perfusion. Structural changes of small resistance arteries play a significant role in the genesis of increased vascular resistance in hypertension and in the maintainance of high blood pressure values. Studies in humans have demonstrated that minimal vascular resistance can be reduced with the use of different antihypertensive drugs, while a complete normalization of the media: lumen ratio was observed only with ACE inhibitors. Further studies are needed to assess the true clinical impact, in terms of reduced morbidity and mortality of reversal of cardiovascular structural changes in hypertensive patients. However, available studies indicate that reversal of LVH reduces the pathological consequences of increased left ventricular mass, and preliminary data suggest that complete regression of LVH may be associated to a decreased risk for cardiovascular events.

Antihypertensive Agents↗