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Biomedical subjects

P Städler

Publications and source records attributed to P Städler.

6 recordsLinked to original sources
PubMed1988

Sodium and responses to infused noradrenaline and angiotensin II in subjects predisposed to hypertension.

A disturbed adrenergic dependent blood pressure regulation may represent a familial component in the pathogenesis of essential hypertension; its possible relation to sodium metabolism is presently unknown. Body sodium, the cardiovascular pressor reactivity to infused noradrenaline or angiotensin II, plasma levels of noradrenaline, adrenalin, renin, angiotensin II, aldosterone and atrial natriuretic peptide were measured on a low or high sodium diet in 10 normotensive young subjects without and 13 normotensive subjects with familial predisposition to hypertension. On the low sodium diet, the two groups did not differ significantly in the considered parameters, while blood pressure was slightly higher in predisposed subjects (+7/+7 mmHg). The change from the low to the high sodium diet was associated with a significant increase in supine systolic blood pressure in predisposed but not in non-predisposed subjects (P less than 0.05). Exchangeable sodium, body weight atrial natriuretic peptide and the pressor reactivity to infused adrenalin or angiotensin II increased significantly while plasma catecholamines, renin, angiotensin II and aldosterone levels were suppressed to a comparable extent in the two groups. The findings of this investigation confirm that sodium has an important regulatory effect on cardiovascular pressor responsiveness. The disturbed noradrenergic-dependent regulation of predisposed subjects is not explained by an abnormal adaptation of sympathetic dependent mechanisms or of other pressor factors to variations in dietary sodium intake.

Adult↗
PubMed1988

Blunted aldosterone responsiveness to angiotensin II in normotensive subjects with familial predisposition to essential hypertension.

The responsiveness of plasma aldosterone to an angiotensin (Ang) II infusion was assessed in normotensive young men, nine without and 13 with a family history of essential hypertension, after 7 days of low (mean urinary sodium 12 +/- 10 mmol/24 h) and 7 days of high (269 +/- 92 mmol/day) sodium intake. Under both conditions, the two study groups did not differ in body weight, arterial pressure, heart rate, plasma or urinary sodium and potassium or plasma renin, aldosterone or Ang II levels. However, after both dietary periods, the relationship between plasma aldosterone and plasma Ang II concentrations had shifted significantly (P less than 0.01) to the right in predisposed compared to non-predisposed subjects. The sodium-related changes in adrenocortical sensitivity to Ang II were similar in the two groups. The pressor response to Ang II did not differ between the two groups of subjects. These findings suggest that, in addition to the known cardiovascular abnormalities of sympathetic, renal and ion transport mechanisms, a fourth area of disturbance involving the response of plasma aldosterone to Ang II may be present in normotensive subjects with familial predisposition to essential hypertension.

Adrenal Cortex↗
PubMed1987

Cardiovascular effects of verapamil in essential hypertension.

Calcium antagonists may affect the regulation of body sodium and adrenergic-dependent mechanisms. Exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, pressor responsiveness to norepinephrine, heart rate responses to isoproterenol, and lipid metabolism were studied in 15 patients with essential hypertension after 8 weeks of treatment with verapamil (348 +/- 68 (SD) mg/day). Supine blood pressure decreased from 153/103 +/- 19/12 mm Hg to 140/95 +/- 14/12 mm Hg (P less than 0.01). Exchangeable sodium, blood volume, plasma norepinephrine, renin and aldosterone, serum total cholesterol, the lipoprotein fractions, and apoprotein levels were unchanged. The norepinephrine pressor and the isoproterenol chronotropic doses tended to increase, whereas the dose-response curve of blood pressure related to plasma norepinephrine was significantly displaced to the right (F = 5.34; P less than 0.05). The antihypertensive effect of verapamil is associated with a decreased cardiovascular pressor responsiveness to norepinephrine without changes in endogenous noradrenergic activity. Moreover, verapamil does not modify the sodium/fluid volume state, the activity of the renin-angiotensin aldosterone axis, or lipid metabolism.

Adult↗
PubMed1987

Renal tubular handling of sodium and familial predisposition to essential hypertension.

Renal clearance of lithium and sodium, glomerular filtration rate, renal plasma flow and certain other parameters of proximal tubular function were determined in 10 normotensive men without, and 13 normotensive men with a family history of essential hypertension after a low- and high-sodium diet. Under low-sodium conditions, the two groups did not differ in mean body weight, exchangeable sodium, plasma renin activity, clearances of inulin, para-aminohippurate (PAH), lithium, sodium, potassium, uric acid or inorganic phosphate, although blood pressure tended to be slightly, but not significantly, higher in those with a family history of hypertension. After changing to the high sodium diet, body weight, exchangeable sodium, and sodium clearance increased and renin decreased significantly (P less than 0.05) and to a similar extent in the two groups; systolic blood pressure increased only in subjects with a family history of hypertension. In both groups renal clearances of inulin, PAH, lithium, potassium, uric acid and inorganic phosphate remained unchanged. These findings do not support the concept that familial predisposition to hypertension is associated with an enhanced proximal reabsorption of sodium. Moreover, the pressor response to a high sodium intake in predisposed subjects is not mediated by an abnormal adaptation of renal sodium metabolism.

Adult↗
PubMed1986

Blood pressure regulation on low and high sodium diets in normotensive members of normotensive or hypertensive families.

In members of hypertensive families a high sodium intake may have a pressor effect. The mechanism mediating the sodium sensitivity is unclear. Blood pressure, exchangeable sodium, plasma levels of norepinephrine, epinephrine, renin and aldosterone, the pressor response to infused norepinephrine or angiotensin II and the urinary excretion of prostaglandin (PG) E2 and F2 alpha were measured after 7 days of low sodium diet (urinary sodium 13 +/- 10 s.d. mmol/24 h) and 7 days of high sodium intake (urinary sodium 268 +/- 97 mmol/24 h) in 10 normotensive men without and 13 men with family history of essential hypertension. After the low sodium phase, blood pressure, heart rate, exchangeable sodium, plasma levels of norepinephrine, epinephrine, renin and aldosterone, pressor doses of norepinephrine or angiotensin II and the urinary excretion of PGE2 or PGF2 alpha did not differ between the two groups. After the high sodium phase, blood pressure increased only in subjects with positive (P less than 0.05) but not in those with negative family history. In the two groups exchangeable sodium increased (P less than 0.05) and plasma levels of NE (-33% versus -32%), renin (-31% versus -27%) or aldosterone (-74% versus -61%) and pressor doses of NE (-55% versus -54%) or ANG II (-72% versus -44%) decreased by a comparable extent. Urinary PGE2 or PGF2 alpha were unchanged. These findings suggest that a high dietary sodium intake exerts a pressor effect in subjects with familial predisposition to essential hypertension. This pressor effect is not explained by an abnormal adaptation of body sodium, sympathetic activity, renin-angiotensin-aldosterone axis, cardiovascular pressor responsiveness and renal prostaglandin excretion to a high sodium diet.

Adult↗