PubMed Health⌕ Search

Biomedical subjects

R Garcia-Robles

Publications and source records attributed to R Garcia-Robles.

15 recordsLinked to original sources
PubMed1997

Sympathoexcitatory effect of hypothalamic/hypophysary inhibitory factor in rats.

We recorded changes in arterial blood pressure, heart rate, and renal sympathetic nerve activity in response to intracerebroventricular injection of bovine hypothalamic/hypophysary inhibitory factor and ouabain in conscious Wistar rats. Ouabain at 0.3 to 0.6 microgram caused dose-related increases in blood pressure, heart rate, and nerve activity (peak increases: 19 +/- 2 mm Hg, 42 +/- 4 beats per minute, and 48 +/- 4%, respectively; P < .05 versus basal). These responses were all blocked by central antibody Fab fragments, which bind ouabain and related steroids with high affinity. The inhibitory factor significantly increased blood pressure but decreased heart rate and nerve activity. Dose-dependent increases in blood pressure as well as heart rate and nerve activity were observed when the inhibitory factor was injected after intravenous injection of the vasopressin antagonist D-(CH2)5Tyr-(Me)AVP. Central Fab fragments, however, did not affect these responses. Both ouabain and the inhibitory factor inhibited Na+,K+-ATPase activity in vitro. Fab fragments blocked this inhibition by ouabain but not by the inhibitory factor. These data indicate that the ouabainlike sympathoexcitatory effect of this factor is masked probably by a potent central effect on vasopressin release. In contrast to rat brain "ouabain," this factor does not exhibit a high affinity for the Fab fragments, supporting the previous finding that this compound is structurally a nonouabain Na+,K+-ATPase inhibitor.

Animals↗
PubMed1997

Comparative effect of PGE2 and PGI2 on renal function.

Rapid degradation of prostacyclin (PGI2) inherent to its molecular structure has long been a major limitation in assessing the natriuretic effect of this prostaglandin. The recent availability of the stable PGI2 analogue iloprost now allows for a comparative study with prostaglandin E2 (PGE2). In the present study conducted in six anesthetized dogs, the intrarenal effects of two consecutive doses (1 and 4 ng x kg(-1) x min(-1)) of PGE2 on renal blood flow, glomerular filtration rate, and urinary sodium excretion were compared with the effects of two identical doses of iloprost. The selected doses of PGE2 were those producing a maximal natriuretic and vasodilator response without affecting mean arterial pressure. A washout period was allowed between administration of PGE2 and iloprost. PGE2 infusion significantly increased fractional sodium excretion from 0.69+/-0.1 to 2.79+/-1.1% and 4.27+/-1.2%% (P<.05), respectively. These changes in fractional sodium excretion induced by PGE2 were associated with significant increases in renal blood flow from 151.1+/-62 to 185+/-64.3 and 185.6+/-64.3 mL/min (P<.05), respectively; however, no significant alterations were seen in glomerular filtration rate, from 29.5+/-9.4 to 35.2+/-12.2 and 32.7+/-7.8 mL/min (NS), and mean arterial pressure, from 117.6+/-26 to 113.9+/-24.1 and 112.3+/-24.1 mm Hg (NS) during control and PGE2 infusion. At identical doses, sequential infusion of PGI2 had no effect on renal blood floww and glomerular filtration rate, producing natriuresis only at the highest dose, a fractional sodium excretion from 0.69+/-0.1 to 0.8+/-0.28 mm Hg (NS) and 1.05+/-0.34% (P<.05), respectively. In conclusion, the present study confirms that PGE2 exerts a natriuretic effect during increases in renal blood flow. In contrast, PGI2 had no hemodynamic effect, and the natriuresis was markedly blunted.

Animals↗
PubMed1996

Aging abolishes the renal response to L-arginine infusion in essential hypertension.

A defect in the endothelium-dependent vasorelaxation could contribute to the development of arterial hypertension through the facilitation of renal vasoconstriction and sodium retention. In this study, we tested the hypothesis that aging impairs kidney function in essential hypertension through a derangement of nitric oxide-dependent renal mechanisms. To this end, we compared the renal response to an intravenous infusion of the precursor of nitric oxide synthesis, L-arginine, in young and aged essential hypertensives. In young hypertensives, L-arginine induced a significant increase in renal plasma flow, glomerular filtration rate, natriuresis and kaliuresis, without changes in filtration fraction. These effects were not observed in aged hypertensives. Neither PRA nor PA were affected by L-arginine infusion in any group. These results indicate that aging produces a derangement of endothelial function in essential hypertension.

Adult↗
PubMed1993

Properties of the purified hypothalamic pituitary NA/K-ATPase inhibitor.

Previously we described the isolation and final purification of an endogenous sodium-pump inhibitor from the CNS, mainly from bovine hypothalamus and pituitary. The purification protocol consisted of lipophilic chromatography, followed by lipid extraction, and semipreparative and analytical reverse-phase high-pressure liquid chromatography. The bioassays used were in vitro Na+/K(+)-ATPase inhibition, and 3H-ouabain displacement from its specific binding site in the enzyme structure, as well as inhibition of 86Rb uptake from human red blood cells. We have obtained, from both tissues, a low-molecular-weight, nonpeptidic, nonlipidic substance that elutes as a single peak highly pure according to criteria of coincidence of its spectra properties. When rechromatographed in two different chromatographic systems, the same homogeneous peak is obtained suggesting complete purity. This pure substance can be isolated from other bovine tissues as well as from human plasma and human placenta. It shows a very distinctive fluorescence spectrum and it behaves as a potent inhibitor of the Ca2+ pump of synaptosomal plasma membrane.

Animals↗
PubMed1989

Effects of nisoldipine on renal function in normal volunteers and essential hypertensive patients.

To evaluate the renal effects of nisoldipine (N), a dihydropyridine derivative, we have evaluated the variations of blood pressure (BP), heart rate, glomerular filtration rate (GFR), renal plasma flow (RPF), 24-h natriuresis, and renal capacity to excrete an i.v. sodium load (2,000 ml isotonic saline in 4-h) in response to a 4-day course of therapy with placebo (P) and N in six normotensive volunteers and six mild-to-moderate essential hypertensive patients. Both volunteers and patients were studied on two constant diets (20 and 150 mEq of sodium daily). No parameters changed after P. On the contrary, N induced a significant fall of BP (p less than 0.01) in the group of patients but not in volunteers. In both groups RPF and GFR increased significantly (p less than 0.05-0.01) while on a low sodium intake but remained constant when sodium intake was high. In the two groups studied, nisoldipine exhibited natriuretic properties manifested by an increase in the 24-h output of sodium as well as by an increased renal capacity to excrete the i.v. sodium load. These natriuretic properties were present in both situations of sodium load and could be facilitated by the change in renal hemodynamics observed when the intake of sodium was low.

Adult↗
PubMed1987

Pharmacological influences on aldosterone secretion.

Besides the classical modulators of aldosterone secretion, new factors influencing positively or negatively aldosterone secretion have been described. These new factors and the effect of related drugs constitutes the aim of this review. The effect of dopamine agonists and H2-receptor antagonists on aldosterone secretion in normal volunteers as well as in different clinical situations characterized by an increased production of aldosterone opens a new field of investigation for the therapy of aldosterone secretion alterations.

Aldosterone↗
PubMed1987

Dopaminergic modulation of aldosterone secretion in the normal menstrual cycle.

A group of eight normotensive female volunteers with regular menstrual cycles were studied during two menstrual cycles: a control cycle and one in which they received lisuride, a D1-D2 dopamine agonist (0.025 mg/8 hr). The following tests were performed in both halves of both cycles: 1) the response of prolactin (PRL) to thyrotropin-releasing hormone (TRH) administration; 2) the response of plasma renin activity (PRA) and plasma aldosterone (PA) to furosemide for 2 hours in the upright posture; and 3) the response of PRL, PRA, PA, plasma potassium (K), and cortisol (F) to metoclopramide administration. An increased response of PRL to TRH and PA to furosemide in the upright position and to metoclopramide were found in the luteal phase of the control study (p less than 0.05). After lisuride administration, in the interphase, differences in the responses of PRL to TRH and PA to furosemide in the upright position disappeared, whereas that of PA to metoclopramide increased further. We conclude that the increase of aldosterone normally observed during the luteal phase of the menstrual cycle is at least partly conditioned by diminished dopaminergic tone and that the response of aldosterone secretion to furosemide-induced sodium depletion and its response to metoclopramide stimulation may be modulated by two different types of dopamine receptors.

Adult↗
PubMed1985

Influence of lisuride, a dopaminergic agonist, on the sexual function of male patients with chronic renal failure.

The effects of Lisuride, a dopaminergic agonist, on the levels of plasma prolactin (PRL), testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and on the variations of libido and coital frequency of patients with chronic renal failure (CRF) have been investigated in a group of 20 male patients (ten normoprolactinemic and ten hyperprolactinemic). Ten patients were included in a hemodialysis program and another ten received conservation therapy (all had creatinine clearance rates below 15 mL/min). The response of PRL to TRH administration and that of LH and FSH to LH-RH administration have also been studied. Low levels of plasma testosterone found initially in all the patients, increased in both normoprolactinemic (P less than 0.05) and hyperprolactinemic patients (P less than 0.01) during Lisuride administration. PRL decreased (P less than 0.01) in both groups during therapy. The increase of plasma testosterone was greater in hyperprolactinemic patients (86% v 15% in normoprolactinemic) and was accompanied by a clear improvement in the studied parameters of sexual behaviors. The response of PRL to TRH was modified in hyperprolactinemic patients while that of LH and FSH to LH-RH was not modified, although Lisuride induced an increase of the basal value of LH (P less than 0.01) in the hyperprolactinemic group. The drug was fairly well tolerated, did not induce hypotension, and the overall incidence of side effects decreased along the study. These results stress the need for further studies with this agent in patients with chronic renal failure and sexual dysfunction.

Adult↗
PubMed1984

Failure of angiotensin II to reduce plasma renin activity in hypertensive pregnant women.

The hypothesis that pregnancy induced hypertension (PIH) is associated with abnormal physiological control of plasma renin activity (PRA) was tested by studying the effects of graded infusion of angiotensin II (ANG II) on PRA, plasma aldosterone (PA), and blood pressure in normal pregnancy, PIH, non-pregnant women in luteal and follicular phase of the menstrual cycle, and males. PIH occurring in the second trimester was associated with elevated PRA, PA and blood pressure compared with all other groups, and reduced urinary thromboxane excretion compared with normal pregnancy. Exogenous ANG II infusion failed to suppress existing PRA in patients with PIH, in contrast to all other groups, but increased PA in all groups. It is concluded that PIH occurring in the second trimester is associated with elevated PRA, PA and blood pressure. The inability of circulating ANG II to reduce PRA in PIH may constitute a major alteration underlying the pathophysiology of PIH.

Adult↗
PubMed1983

Participation of renal prostaglandins in the nephrotic syndrome.

The participation of renal prostaglandins in the nephrotic syndrome has been investigated by the measurement of the urinary excretion of prostaglandin E2 (PGE2), renal function and the renin-angiotensin-aldosterone system before, during and after the administration of indomethacin in a group of patients diagnosed as having chronic idiopathic glomerulonephritis with and without nephrotic syndrome. Our results indicate increased renal production of PGE2 in nephrotic patients. This contributes to the maintenance of renal function, probably by counteracting an activated renin-angiotensin system and could be accompanied by a simultaneous and deleterious enhancement of the degree of proteinuria. Nevertheless, the participation of angiotensin II in this last even cannot be excluded.

Adolescent↗
PubMedDate not supplied

Effect of furosemide on renal function in the stenotic and contralateral kidneys of patients with renovascular hypertension.

In a group of six patients diagnosed as having unilateral renovascular hypertension due to fibromuscular dysplasia, inulin glomerular filtration rate, (GFR) and PAH renal plasma flow, (RPF) clearances, urine flow (V), urine sodium (UVNa), potassium (UVK), urinary excretion of prostaglandin E2 (UVPGE2), thromboxane B2 (UVTxB2), and 6-keto prostaglandin F1 alpha (UVPGF1 alpha) were measured in each kidney before and after the i.v. administration of furosemide (20 mg). The basal values of GFR, RPF, UVNa, UVPGE2, UVTxB2, and UV6-keto-PGF1 alpha were lower (p less than 0.01) in the stenotic kidney. Furosemide increased RPF 11% and 50%, GFR 25% and 62%, and V 142% and 280% in the contralateral and stenotic kidney respectively. The increase of UVNa was similar in the two kidneys. In the stenotic kidney, both UVPGE2 and UV6-keto-PGF1 alpha increased significantly (p less than 0.01) with furosemide while UVTxB2 remained unchanged. Furosemide did not alter the rate of excretion of the three prostaglandins measured in the contralateral kidney. We conclude that furosemide significantly improves renal circulatory and excretory function of the stenotic kidney. Since prostaglandin excretions also increased, the vasodilatation in the stenotic kidney may be prostaglandin mediated.

Adult↗