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Biomedical subjects

J Ribstein

Publications and source records attributed to J Ribstein.

At least 127 records · Page 7Linked to original sources
PubMed1985

Effect of chronic nifedipine in patients inadequately controlled by a converting enzyme inhibitor and a diuretic.

Nifedipine, in a slow release preparation, was given at a mean daily dosage of 47 +/- 4 mg to 12 patients with severe hypertension in whom arterial pressure was not satisfactorily controlled (mean arterial pressure 132 +/- 4 4 mm Hg) by the combination of a converting enzyme inhibitor and a diuretic. The addition of nifedipine induced an appreciable decrease in mean arterial pressure of 31 +/- 5 mm Hg and of serum potassium and plasma aldosterone. After adequate control of hypertension and because of severe hypokalemia in some patients, discontinuation of the diuretic was attempted in 10 subjects. After 1.7 +/- 0.5 months of treatment by the converting enzyme inhibitor and nifedipine no change in arterial pressure occurred while serum potassium had returned to normal in most patients. These results show that nifedipine may be useful in patients with a residual rise of arterial pressure when treated by converting enzyme inhibitor plus diuretics; in such patients, however, the serum potassium concentration should be carefully monitored. In addition, our observations suggest that calcium blockers may be an effective alternative to diuretics in patients receiving a converting enzyme inhibitor.

Adult↗
PubMed1985

Renal effects of calcium blockade by tiapamil in normal and hypertensive subjects.

The acute hypotensive and renal effects of the calcium antagonist tiapamil, a verapamil derivative, were studied in nine normal and 13 essential hypertensive subjects undergoing water diuresis. Tiapamil decreased mean arterial pressure slightly in normotensive subjects and more markedly in hypertensive patients (-6 +/- 1 versus -10 +/- 2%). The effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) were unaffected in both groups. A striking natriuresis was observed selectively in the hypertensive group (+344 +/- 84 versus +42 +/- 22 mmol/min) and was associated with an increase in the calculated fractional distal delivery of sodium and uric acid excretion rate. Plasma aldosterone concentration decreased moderately and to the same extent in both groups. In conclusion, tiapamil induced a marked natriuresis in essential hypertensive patients, despite a decrease in blood pressure, and in the absence of renal vasodilatation; this may suggest the existence in essential hypertension of a calcium-linked abnormality in the renal proximal tubular handling of sodium.

Adult↗
PubMed1985

Reflex responses to reductions in functioning renal mass.

Both acute unilateral nephrectomy (AUN) and unilateral ureteral obstruction (UUO) result in an acute increase in cation excretion from the contralateral kidney. AUN results in reflex changes in systemic hemodynamics owing to an acute and transient increase in arterial pressure that activates carotid sinus baroreceptors and constitutes an afferent limb in the reflex; hemodynamic adjustments and increased cation excretion result. The reflex involves participation of the endogenous opioid system, with receptors located primarily in the central nervous system, and requires intact pituitary function because both hypophysectomy and pretreatment with large doses of dexamethasone prevent the postnephrectomy natriuresis. The natriuresis is closely correlated with an increase in the plasma concentration of the NH2-terminal fragment of the pituitary peptide precursor molecule proopiomelanocortin, which suggests that such a peptide could participate directly or indirectly in the postnephrectomy natriuresis. Surgical denervation of either the ipsilateral or the contralateral kidney markedly alters the response to AUN, which prevents the natriuresis and blunts the kaliuresis, and indicates a role for renal neural reflexes. Renorenal reflex pathways also mediate the response of the contralateral kidney to UUO, because denervation of either the ipsilateral (obstructed) or the contralateral kidney abolishes both the natriuresis and kaliuresis usually seen after UUO. This reflex also involves the endogenous opioid system, for it does not occur in rats receiving an i.v. infusion of the opiate receptor antagonist naloxone.

Adaptation, Physiological↗
PubMed1985

[Acute effect of nifedipine on arterial pressure and the renin-angiotensin system in healthy subjects and hypertensives].

The acute effects of nifedipine (20 mg capsules) on the blood pressure and renin-angiotensine system were studied in 108 subjects, 25 normotensives, 51 borderline hypertensives and 33 permanent essential hypertensives. The fall in mean blood pressure (MBP) was rapid (less than 30 minutes) and significant in all groups; the amplitude the hypotensive response expressed as a percentage of the basal MBP was directly related to the basal MBP value (r = 0.54, p less than 0.001). The amplitude of the response correlated with the control plasma renin activity only the group with permanent hypertension (r = - 0.40, p less than 0.025). The fall in blood pressure and the reflex sympathetic stimulation induced by nifedipine were not associated with an increased plasma renin activity. The plasma aldosterone concentrations varied only in the group of permanent hypertensive patients after nifedipine ( - 4 +/- 1 ng/dl, p less than 0.01).

Adolescent↗
PubMed1984

Renal nerves and cation excretion after acute reduction in functioning renal mass in the rat.

We evaluated the role of the renal nerves in the increased cation excretion by the contralateral kidney after acute unilateral nephrectomy (AUN) or unilateral ureteral occlusion (UUO) in anesthetized rats. Both AUN and UUO caused large increases in sodium (UNaV) and potassium excretion (UKV) by the control kidney without change in glomerular filtration rate or mean arterial pressure. Prior denervation of either the ipsilateral (experimental) kidney or the control kidney completely prevented the increase in UNaV and UKV after UUO. Prior denervation of either kidney also prevented the increase in UNaV after AUN. However, a significant kaliuresis persisted after AUN despite unilateral denervation although reduced in magnitude when compared with the increase in UKV after AUN with both kidneys innervated. These results indicate that the renal nerves play a major role in the excretory response of the control kidney after acute reduction in functioning renal mass. This role of the renal nerves may be through the activation of a renorenal reflex. The reflex is activated by afferents from the ipsilateral kidney; the efferent limb is composed of the renal nerves to the control kidney. This reflex can entirely account for the compensatory increase in cation excretion after UUO. However, a separate mechanism, not dependent on the renal nerves, contributes to UKV after AUN.

Animals↗
PubMed1983

Endogenous opioids and electrolyte excretion after contralateral renal exclusion.

Acute reductions in functioning renal mass result in increases in both sodium (U Na V) and potassium (U K V) excretion by the contralateral kidney (CK). We studied the role of endogenous opioids in this response. In control experiments acute unilateral nephrectomy (AUN) increased U Na V from 1,788 +/- 1,125 (SD) to 3,939 +/- 1,819 and U K V from 1,385 +/- 561 to 2,254 +/- 832 neq/min by the CK (P less than 0.005 for both); similar results occurred in rats undergoing acute unilateral ureteral occlusion (UUO). These increases occurred without overall change in GFR or mean arterial pressure. In rats receiving a continuous infusion of the opiate-receptor antagonist naloxone (0.3 mg . kg-1 . h-1) neither AUN nor UUO produced significant alterations in U Na V or U K V by the CK; naloxone infusion by itself did not alter GFR or basal rates of cation excretion. A separate group of rats was made tolerant to morphine by subcutaneous implantation of pellets containing 75 mg morphine base. In these rats, AUN also failed to produce any increase in U Na V or U K V by the CK. The results suggest that acute reductions in functioning renal mass produced by either AUN or UUO stimulate cation excretion by the remaining kidney through reflex pathways that involve opiate receptors.

Animals↗
PubMed1982

[Haemorrhagic necrosis of a pituitary adenoma in a case of multiple endocrine neoplasia (author's transl)].

A case of pituitary adenoma in a 55 years old man was revealed by sudden pituitary apoplexy due to haemorragic necrosis of the tumor. Neurological signs were intracranial hypertension, epistaxis and evolutive bilateral ophtalmoplegia. Case history revealed a multiple endocrine neoplasia including a pancreatic insuloma and a parathyroïd adenoma. Biological data were hypercalcemia, hypophosphoremia and elevated serum levels of prolactine and parathormone. The characteristic features of pituitary haemorragic necrosis and multiple endocrine neoplasia are reviewed.

Hemorrhage↗
PubMed1981

[Type I multiple endocrine neoplasia with prolactin-secreting tumor revealed by pituitary apoplexy (author's transl)].

Prolactin-secreting adenoma is probably the most common functional pituitary tumour in type I multiple endocrine neoplasia (MEN I). The authors report on a case of gastrinoma and parathyroid adenoma associated with prolactinoma. The latter tumour was revealed by sudden pituitary apoplexy. The characteristic features of endocrine tumours in MEN 1 are discussed, and the relevant literature is reviewed. Emphasis is placed on the fact that prolactinomas are well tolerated, remain clinically silent for a long time and may be diagnosed only when dramatic symptoms suddenly appear.

Cerebrovascular Disorders↗
PubMed1981

Effect of captopril on the systemic and renal responses to acute isotonic volume expansion in normal man.

Systemic, humoral and renal responses to isotonic volume expansion (VE, 1800ml in 3 hours) were assessed in normal subjects before and during captopril administration (CEI). Captopril, which otherwise induced a decrease in pre-saline mean arterial pressure (MAP) unmasked the volume-dependence of MAP since during captopril administration MAP increased linearly during volume expansion (+18.7 +/- 3.8% at the end of VE). In addition, captopril prevented the fall in plasma aldosterone produced by VE but did not modify the natriuretic response to saline. These results demonstrate that circulating angiotensin II is not an important determinant of the natriuretic response to volume expansion in normal man. However, a role for intrarenal renin cannot be excluded.

Adult↗
PubMedDate not supplied

Albuminuria in normals and essential hypertension.

The prevalence and determinants of urinary albumin excretion rate (AER) were assessed in lean and overweight normotensive subjects (NT) and patients with essential hypertension (EH). In NT and EH, the presence of overweight was associated with a significant exacerbation of AER. In the normotensive population, AER was higher in subjects with a positive family history of hypertension. An important role for smoking was observed in the hypertensive population; in fact, the prevalence of microalbuminuria (MA) was almost twofold in lean hypertensive smokers when compared to nonsmokers. Among other determinants of AER, a major influence of systolic arterial pressure, urinary excretion of urea (an estimate of protein intake), and high-density lipoprotein (HDL) cholesterol (inversely correlated with AER) was observed mainly in lean EH patients. The significance of microalbuminuria is unclear. Is it a marker of cardiovascular risk and/or a predictor of the future development of renal disease in EH?

Adolescent↗
PubMedDate not supplied

Comparative effect of captopril and nifedipine in normotensive patients with incipient diabetic nephropathy.

In these studies, the effect of a 6-wk treatment by placebo, the calcium-channel blocker nifedipine, or the converting-enzyme inhibitor captopril was assessed in normotensive patients with insulin-dependent diabetes and incipient nephropathy. In response to captopril and nifedipine, arterial pressure decreased slightly and to a similar extent. These drugs resulted in opposite effects on urinary excretion of albumin [i.e., increase in urinary albumin excretion (UAE) by 40% during nifedipine treatment and decrease by 40% during captopril treatment]. No change in UAE was observed in the placebo group. This observation of opposite changes in UAE in the presence of a similar fall in arterial pressure suggests that the effects of captopril and nifedipine on UAE result from some difference in their intrarenal action. The data do not present recommendations for the use or disuse of captopril or nifedipine in such a group of patients and do not allow extrapolation to hypertensive diabetic subjects well controlled by other conventional antihypertensive agents.

Adult↗
PubMedDate not supplied

Angiotensin II receptor antagonists and hypertension.

Over recent years, a number of imidazole derivatives that specifically bind to the angiotensin II type 1 receptor, thereafter called sartans, have been developed and made available to the clinician. Whether targeting antihypertensive treatment with such a high specificity within the renin cascade may carry major clinical advantage over inhibiting angiotensin converting-enzyme remains to be demonstrated. In short-term studies, the efficacy of these drugs at reducing blood pressure was similar to that of established comparators, whereas overall side effect profile was comparable to that of placebo.

Angiotensin II↗