Evidence for distal tubular inhibition of calcium efflux by nisoldipine in the SHR rat.

Nisoldipine, a calcium channel blocking agent, is known to have antihypertensive, renal tubular and hemodynamic effects. The present studies were designed to examine the effects of this drug on the renal tubular transport of calcium in 12 saline-loaded SHR rats. Calcium-45 was infused into three different nephron segments: early proximal, late proximal and early distal sites with or without nisoldipine.

Renal response to volume expansion in streptozotocin-induced diabetic rats: influence of calcium channel blockade.

The renal response to volume expansion (VE) has been shown to be impaired in streptozotocin (STZ)-induced diabetes. This may contribute to the abnormal maintenance of fluid balance in diabetics. Since calcium channel blockade (CaCb) has been shown to improve renal hemodynamic and tubular functions, the present studies were designed to examine the ability of CaCb to enhance the response of kidneys from diabetic rats to a volume load.

Normalization of pressure-natriuresis by nisoldipine in spontaneously hypertensive rats.

This study examined whether the calcium antagonist nisoldipine can shift the relations between sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure toward lower pressures in spontaneously hypertensive rats. Mean arterial pressure decreased similarly by 9% and 12% in Wistar-Kyoto and spontaneously hypertensive rats after nisoldipine (0.5 microgram/kg bolus + 0.

Post-obstruction diuresis: influence of renal prostaglandins.

The possible role of altered renal prostaglandin metabolism in the generation of post-obstruction diuresis (POD) was examined in 16 adult male Sprague-Dawley rats. Inhibition of cyclooxygenase by the administration of a combination of two nonsteroidal anti-inflammatory drugs (NSAID), meclofenamate and indomethacin in 8 of these rats exaggerated, rather than lowered the degree of natriuresis and diuresis that followed the release 24 h after bilateral ureteral ligation. Urine osmolarity was similar in the two groups of rats treated with the NSAID and vehicle.

Blunting of the renal response to volume expansion by a bradykinin receptor antagonist: influence of denervation.

The interaction of renal sympathetic nervous influences with the intrarenal kallikrein-kinin system was examined during graded expansion of the extracellular fluid volume in rats. One group of rats was pretreated with a specific and highly efficacious competitive antagonist of bradykinin receptor (BKRA), whereas the other group received only a vehicle infusion. The left kidney was denervated in each animal and the right kidney remained intact.

Guanabenz action on renal excretory function in New Zealand genetically hypertensive rats.

The renal action of guanabenz, a centrally acting antihypertensive drug, was evaluated in anesthetized New Zealand genetically hypertensive rats and in normotensive Sprague-Dawley rats using clearance techniques. In high doses (1 mg/kg/hr), the drug lowered systemic blood pressure in the hypertensive rats without reducing glomerular filtration rate. Mean urine flow increased from 2.

Kallidin effect on renal tubular function in meclofenamate- and vehicle-pretreated rats.

The effect of kallidin (lysyl-bradykinin) on the urinary recovery of sodium-22 was examined in anesthetized, volume-expanded rats. Sodium-22 was microinfused into the lumen of late proximal convoluted tubules with and without kallidin (100 pg/ml). Kallidin enhanced mean sodium-22 recovery from a control of 2.

Plasma dilution during transdermal clonidine antihypertensive monotherapy.

In eight hypertensive patients treated with transdermal clonidine for one year, there was plasma dilution, as shown by a reduction in serum sodium, hemoglobin, and serum protein levels. Free water clearance did not change significantly. Plasma dilution was likely sustained by increased water intake due to "dry mouth", as frequently seen with central acting drugs such as clonidine.

Augmentation by aprotinin of the renal response to vasopressin.

We contrasted the renal effects of vasopressin in Brattleboro rats with and without pretreatment with aprotinin (20,000 KIU kg-1). In both treatment groups, vasopressin injected at 3 mU kg-1 sec caused in conscious rats elevation of urine osmolality and reduction of urine flow and urinary excretion of total solutes. However, these effects of vasopressin were significantly greater in aprotinin pretreated rats than in rats without aprotinin treatment.

Renal tubular effect of nisoldipine, a calcium channel blocker, in rats.

The renal tubular effect of nisoldipine (10 micrograms/kg/h) was evaluated using clearance and micropuncture techniques in spontaneously hypertensive rats made diuretic by i.v. infusion of 2.

Segmental nephron function in rats treated with aprotinin, an inhibitor of kallikrein.

The effects on kidney function of aprotinin, an inhibitor of kallikrein and other serine proteinases, were investigated in rats made diuretic by infusion of 0.9% saline. Late proximal, early distal and late distal tubular fluid samples were collected before and after aprotinin administration (20,000 kallikrein I.

Renal effects of aprotinin, a kallikrein inhibitor in rats in saline diuresis.

Administration of aprotinin, a kallikrein inhibitor, to anesthetized rats infused with 0.9% saline solution to expand the extracellular fluid volume resulted in blunted natriuresis and diuresis. Urine flow declined from 27.

Role of vasopressin in regulation of renal kinin excretion in Long-Evans and diabetes insipidus rats.

To study the relationship between vasopressin and the renal kallikrein-kinin system we measured the rate of excretion of kinins into the urine of anesthetized rats during conditions of increased and decreased vasopressin level. The excretion of immunoreactive kinins in Brattleboro rats with hereditary diabetes insipidus (DI) (24 +/- 3 pg min-1 kg-1) was lower than in the control Long Evans (LE) rats (182 +/- 22 pg min-1 kg-1; P less than 0.05).

Digoxin transport in the distal nephron of rats during saline diuresis.

The nephron segments involved in the renal tubular transport of digoxin and the direction of transport in each segment were evaluated using renal micropuncture techniques in 11 rats made diuretic by i.v. infusion of .

Effect of prostaglandin synthesis inhibitors on clonidine-induced diuresis in rats.

Clonidine is a centrally acting antihypertensive drug that also has marked renal effects. The role of renal prostaglandins in clonidine-induced diuresis was examined in anesthetized and conscious rats. Twelve surgically prepared rats were pretreated with either of two inhibitors of prostaglandin synthesis, indomethacin or meclofenamate (2 mg/kg), while thirteen rats served as controls.

Effect of the converting enzyme inhibitor SQ-20881 on urinary excretion of prostaglandin E2 in the rat: influence of pretreatment with deoxycorticosterone.

The effect of SQ-20881, an inhibitor of the peptidyl dipeptidase that degrades kinins and converts angiotensin I to angiotensin II, on the urinary excretion of immunoreactive prostaglandin E2 (iPGE2) was studied in rats receiving either deoxycorticosterone (DOCA, 5 mg/day s.c.) or sesame oil vehicle for 10 days before and then during the study, DOCA-treated animals had higher urinary excretion of iPHE2 and kallikrein, and lower plasma renin, than did animals injected with oil only.

Renal effects of indanone in dogs and rats: modification by a cyclooxygenase inhibition.

The effects of indomethacin, a PG synthesis inhibitor, on the renal hemodynamic and diuretic responses to indanone were evaluated in 10 rats and 12 dogs. In anaesthetized rats, 50 mg/kg of indanone, an indanyloxyacetic acid diuretic, increased water excretion 20--30 times, sodium excretion 80--100 times, and potassium excretion 4 times, without marked changes in GFR and BP. Indomethacin pretreatment, 2 mg/kg, did not significantly reduce these responses.