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At least 793 records · Page 44Linked to original sources
PubMed1992

Effects of clonidine on renal sympathetic nerve activity, natriuresis and diuresis in chronic congestive heart failure rats.

The differential effects of the alpha-2 adrenergic agonist, clonidine, on blood pressure, renal sympathetic nerve activity (RSNA) and renal responses were investigated in conscious as well as anesthetized congestive heart failure (CHF) rats and normal control animals. After the stepwise increments of i.v. clonidine infusion (5, 15 and 30 micrograms/hr for 1 hr), mean arterial pressure gradually decreased in CHF, but increased significantly in the control animals at the higher doses. Urinary volume, sodium and potassium excretions were significantly higher in the normal control animals after the clonidine 30-micrograms/hr infusion compared with the CHF rats. There were almost immediate decreases in RSNA in both the CHF and control groups. Although the control animals reduced RSNA to about 5%, the CHF rats retained 36.5% of their respective control values after clonidine administration. Base-line plasma immunoreactive atrial natriuretic peptide were increased 7-fold in the CHF rats compared to controls. After clonidine, immunoreactive atrial natriuretic peptide increased more than 3-fold in the normal rats, whereas no changes were observed in the CHF group. Our data show that clonidine decreases RSNA in CHF and that the natriuretic and that diuretic effects of an alpha-2 receptor agonist are blunted in experimental CHF. Furthermore, the different mean arterial pressure response in the CHF and control groups at higher doses of clonidine may suggest down-regulation of the vascular alpha-2 adrenergic receptor in CHF.

Animals↗
PubMed1991

Thiorphan-induced natriuresis in volume-expanded rats: roles of endogenous atrial natriuretic factor and kinins.

Thiorphan, a potent inhibitor of enkephalinase (membrane metalloendopeptidase, atriopeptidase, EC 3.4.24.11) enhanced markedly (+214%) and prolonged the rise in plasma atrial natriuretic factor (ANF) immunoreactivity in anesthetized rats submitted to acute extracellular volume expansion obtained through i.v. injection of a Ringer's solution. These changes were accompanied by marked potentiations of the natriuretic and diuretic responses to the ANF-releasing stimulus, whereas kaliuresis was only slightly affected. Thiorphan also enhanced markedly the biphasic rise in urinary cyclic GMP excretion elicited by volume expansion. All these renal responses to volume expansion in thiorphan-treated rats were significantly reduced by pretreatment with anti-ANF antibodies, suggesting an involvement of the endogenous natriuretic hormone protected against degradation. However, pretreatment with antibradykinin antibodies led to qualitatively similar results, suggesting that the endogenous kinin-generating system in kidney may also participate in the responses to endogenous ANF and their potentiation by the peptidase inhibitor.

Animals↗
PubMed1990

Bumetanide-induced natriuresis and antinatriuresis in the proximal and distal parts of the human nephron. Investigations in acute and chronic bumetanide treatment.

In the present study we used the Li clearance technique to evaluate the effects of submaximal bumetanide infusion on proximal and distal Na reabsorption in healthy volunteers with and without volume and Na replacement. These effects were studied both in chronic bumetanide-treated and in previous nontreated subjects. Li was given as Li carbonate p.o. Glomerular filtration was evaluated by creatinine clearance. Infusion of bumetanide increased fractional Na excretion and fractional Li excretion in the volume-replaced subject. Without volume-replacement bumetanide infusion increased these excretion rates to a significantly lower level. These results suggest that in humans acute submaximal doses of bumetanide cause inhibition of both proximal and distal tubular reabsorption of Na. Along with diuretic-induced volume contraction the natriuretic response is diminished perhaps due to a secondary increase in fractional Na reabsorption which occurs only in the proximal tubular portions of the nephron. In chronic bumetanide-pretreated subjects, however, the fractional Na and Li excretion increased significantly more than in the previous nontreated subjects. Compared to these ion excretions in diuretic-induced Na and volume-depleted subjects the results suggest that a secondary increase in fractional Na reabsorption is developed rapidly during submaximal bumetanide infusion in chronic bumetanide-treated subjects. In the distal part of the nephron, however, the bumetanide-induced increase in Na excretion is much less in the chronic bumetanide-treated subjects than in previous nontreated. Because of these results it is suggested that simple dose-effect relationship for loop-diuretics will be difficult to describe.

Adult↗
PubMed1987

Acute natriuresis induced by inhibition of proximal tubular reabsorption of sodium and water in hypertensives following acute calcium entry blockade with nifedipine.

To elucidate the renal effects and especially the natriuretic properties of calcium entry blockers, we studied the effect of sublingual nifedipine 20 mg in 16 patients with mild to moderate essential hypertension. The lithium clearance technique was utilized and constant infusion technique was employed to measure glomerular filtration rate (GFR) and renal plasma flow (RPF). Nifedipine induced a significant reduction of systolic and diastolic blood pressure and an increase in heart rate. RPF increased and renal vascular resistance fell significantly, whereas GFR was unchanged. A significant increase in diuresis and in clearance of sodium and lithium was seen. The absolute and fractional proximal reabsorption of sodium and water was reduced. The absolute distal reabsorption increased significantly. The results indicate that the natriuretic action of nifedipine in hypertensives is a proximal tubular event.

Blood Pressure↗
PubMed1989

Effects of the intracerebroventricular atrial natriuretic factor on angiotensin II or sodium-induced blood pressure elevation and natriuresis.

We examined the effects of intracerebroventricular (i.c.v.) administration of atrial natriuretic factor (ANF) on pressor and natriuretic responses induced by i.c.v. angiotensin II (Ang II) or hypertonic NaCl in conscious male Wistar rats. The i.c.v. artificial cerebrospinal fluid (CSF) or ANF alone did not cause recognizable changes in mean blood pressure (MBP), urinary volume (UV), or sodium excretion (UNaV). The i.c.v. Ang II or 0.6 M NaCl raised MBP, decreased UV, and increased UNaV. When ANF was administered with Ang II, the Ang II-induced changes in MBP, UV, and UNaV were diminished significantly. ANF also opposed the effects of 0.6 m NaCl, though the effect was significant only in the case of blood pressure. Our results indicate that brain ANF may have antipressor and anti-natriuretic roles.

Angiotensin II↗