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R A Kramp

Publications and source records attributed to R A Kramp.

13 recordsLinked to original sources
PubMed2000

Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat.

In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca(2+) channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca(2+) channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle (n = 10), 0.3 mg/kg body wt N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), 4.5 microg. kg body wt(-1). min(-1) nifedipine (n = 8) alone, or with nifedipine infused before (n = 8), after (n = 8), or coadministered with L-NAME (n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 +/- 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% after L-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered with L-NAME. RBF autoregulation was maintained after L-NAME, but the autoregulatory pressure limit (P(A)) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with L-NAME limited P(A) resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca(2+)-activated K(+) channels also prevented autoregulatory resetting by L-NAME (n = 8). These findings suggest NO inhibits voltage-dependent Ca(2+) channels and thereby modulates RBF autoregulatory efficiency.

Animals↗
PubMed1997

Differential effects of sulindac on renal hemodynamics and function in the rat.

Renal hemodynamics were studied using an electromagnetic perivascular flow sensor in anesthetized rats injected i.v. with vehicle, 5 or 10 mg/kg body weight (b.w.) sulindac. No hemodynamic changes occurred with vehicle (n = 6), but mean arterial pressure was significantly decreased (by 15 mmHg) with sulindac (n = 12). In the 5 mg/kg b.w. sulindac group (n = 7), renal blood flow progressively and significantly increased from 7.88 +/- 0.36 to 8.98 +/- 0.58 ml/min, except during concomitant intrarenal infusion of 3 mg/kg b.w. per h proadifen (n = 7). The pressure limits for efficient and no renal blood flow autoregulation remained unchanged (approx. 100 and 80 mmHg, respectively). In the 10 mg/kg b.w. sulindac group (n = 5), renal blood flow did not change but autoregulatory pressure limits were lowered by 10 mmHg 2 h after treatment (P < 0.025). Also, Na+ retention was marked. Prostanoid excretion in urine was significantly reduced with either dose but basal plasma renin activity was not (about 8 ng/ml per h; n = 15). When plasma renin activity was enhanced after a reduction in renal perfusion pressure (n = 21), it was decreased from 11.5 +/- 1.2 to 7.4 +/- 0.2 ng/ml per h only by 10 mg/kg b.w. sulindac (P < 0.05; n = 6). In conclusion, differential effects of sulindac on renal hemodynamics, Na+ excretion and plasma renin activity were demonstrated. Renal hemodynamic changes could be related in part to the cytochrome P-450 arachidonic acid pathway.

Animals↗
PubMed1995

Renal hemodynamics and blood flow autoregulation during acute cyclooxygenase inhibition in male rats.

After the acute inhibition of prostanoid synthesis, adjustments of renal hemodynamics may not be characterized immediately. Therefore, time-related effects of indomethacin on hemodynamics and renal blood flow (RBF) autoregulation were studied in anesthetized euvolemic male rats injected intravenously with vehicle, indomethacin (3, 4, or 5 mg/kg body wt), or meclofenamate (4 or 5 mg/kg body wt). Hemodynamics and RBF autoregulation were not influenced by vehicle injection, nor by time (n = 6). In contrast, mean arterial pressure (MAP) decreased significantly from 117 +/- 4 to 103 +/- 3 mmHg, and RBF progressively and significantly increased from 8.00 +/- 0.34 to 9.17 +/- 0.50 ml/min in the 3 mg/kg body wt indomethacin group (n = 8). Treatment with the higher doses of indomethacin (n = 9) or meclofenamate (n = 6) did not change RBF, while MAP decreased by 15 mmHg. A time-dependent significant enhancement of RBF autoregulatory efficiency was found in the drug-treated rats. Changes in renal function and reductions of prostanoid excretion in urine, of plasma renin activity, or serum aldosterone were similar in the nonsteroidal antiinflammatory drug groups. In conclusion, our findings demonstrate important time-related adjustments of renal hemodynamics in male rats treated with indomethacin, especially with the lower dose (3 mg/kg body wt iv). The factor(s) responsible for the hemodynamic changes remains unknown.

Aldosterone↗
PubMed1985

Effects of the diuretic torasemide on p-aminohippuric acid transport in the rat.

The effect of torasemide, a new diuretic, on p-aminohippuric acid (PAH) transport (TPAH) was studied using renal clearance and micropuncture techniques in anaesthetized rats. In clearance experiments, TPAH and TPAH/glomerular filtration rate (GFR) did not significantly change after i.v. administration of torasemide or furosemide but decreased after probenecid injection. In order to enhance the possibility to demonstrate torasemide and PAH interference, small volumes of [3H]-PAH + [14C]-inulin solutions were directly injected into the peritubular capillary system using calibrated micropipettes. When the concentration of microinjected PAH was less than or equal to 0.6 mmol/l, fractional recovery of [3H]-PAH from the micropunctured kidney was not significantly decreased by the diuretics in contrast to probenecid. When the concentration of microinjected PAH was greater than or equal to 5 mmol/l, fractional recovery of [3H]-PAH from the micropunctured kidney was significantly decreased by torasemide from 252% (control) to 210% (P less than 0.005), by furosemide to 217% (P less than 0.005), and by probenecid to 205% (P less than 0.01). Under these conditions, differential transit times between [3H]-PAH and [14C]-inulin in the micropunctured kidney were decreased from -15 to -4 s in the presence of torasemide (P less than 0.05). They were slightly but not significantly reduced by furosemide and probenecid. These findings suggest interference, at least to some extent, between torasemide and PAH secretion in the rat kidney.

Aminohippuric Acids↗
PubMed1982

Glucose transport in chronically altered rat nephrons.

Microinjection experiments were performed in anesthetized rats to study the tubular absorptive capacity for glucose (TG) in normal and chronically altered tubules, i.e., tubules that sustained anatomical repair and compensatory changes of their previously normal configuration after acute damage. TG was complete when the glucose load injected in normal or altered early or late proximal convolutions was less than or equal to 1.5 or less than or equal to 10 pmol . s-1, respectively. In normal tubules, TmG was 10 and 5 pmol . s-1 after early and late proximal microinjections, respectively. After early proximal microinjections in altered tubules, different levels of TmG were found. They related to the degree of compensatory growth. TmG was approximately 12, 24, or 35 pmol . s-1, respectively, in altered tubules with minor, moderate, or major compensatory growth. After late proximal microinjections, TmG was 15 pmol . s-1. TG variability was greater in altered than in normal tubules. Correlation between structural and functional compensatory changes was thus demonstrated. Furthermore, an important, albeit latent, absorptive capacity for glucose of the proximal straight tubule was found.

Animals↗
PubMed1975

Distal permeability to urate and effects of benzofuran derivatives in the rat kidney.

Effects of benziodarone and benzbromarone on renal tubular permeability to urate-14C were investigated in anesthetized rats by microinjection and clearance experiments. Urate-14C and inulin-3H were injected into proximal and distal convolutions and their recovery was measured in urine collected serially. In control rats, total and direct recoveries were significantly lower after early proximal (72 and 52%, respectively) than after late proximal injections (83 and 63%), whereas distal recoveries were higher (94 and 69%). Delayed excretion (ca. 25%) did not change with site of injection. Total distal recoveries were always less than 100% (P smaller than 0.001) but increased to 98% at high loads. After proximal injections in drug-pretreated rats, total and direct recoveries increased significantly (P smaller than 0.001). Recoveries after distal injections did not change in benzbromarone-treated rats, whereas direct and delayed excretion, respectively, increased (87%) and decreased (9%) significantly (P smaller than 0.001) following benziodarone infusion. These findings demonstrate inhibition of proximal urate reabsorption by benzofuran derivatives. The results also suggest distal reabsorption of urate, presumably along the collecting ducts.

Animals↗
PubMed1975

Characteristics of urate influx in the rat nephron.

Permeability of the tubular epithelium to urate presented on the peritubular side was studied in anesthetized rats during mannitol diuresis by capillary microinjections of [14C]urate and [3H]inulin, [14C]PAH and [3H]inulin, or [14C]urate and [3H]PAH. Recovery of isotopes was determined in urine collected serially from the injected and contralateral kidney. Appearance and peak excretion of urate in the experimental but not in the contralateral kidney preceded inulin and coincided with PAH, indicating proximal permeability to urate. Recovery of urate was higher from the injected than from the contralateral kidney. Urate precession and recovery did not change after addition of PAH (1.5-6.4 mm) to [14C]urate-[3H]inulin solutions, whereas they decreased significantly in the experimental kidney after pyrazinoate (1.6-3.2 mM) addition. On the other hand, no effect of urate on [14C]PAH-[3H]inulin injections was detectable. These findings are suggestive of a carrier-mediated transtubular influx of urate in rat proximal tubule. Absence of competition with PAH may suggest differences in the secretory mechanisms for organic acids.

Aminohippuric Acids↗
PubMed1971

Urate-2-14C transport in the rat nephron.

Intrarenal transport of urate-2-(14)C was studied in anesthetized rats using the microinjection technic. During saline diuresis, small volumes of urate-2-(14)C (0.24-0.48 mM) and inulin-(3)H were injected into surface proximal and distal convoluted tubules, and ureteral urine was collected serially. Total (74-96%) and direct (57-84%) urate recovery increased significantly the more distal the puncture site. Delayed recovery (+/-20%) remained approximately the same regardless of localization of the microinjection. After proximal injections, total and direct recoveries of urate-2-(14)C were significantly higher in rats treated with probenecid, pyrazinoate, or PAH than during saline diuresis alone, while the excretion rates were comparable after distal injection. Delayed recovery was not altered by drug administration. The decreased proximal reabsorption of urate is presumably due to an effect of the drugs on the luminal membrane of the nephron. For perfusion at high urate concentrations, nonradioactive urate was added to the injectate (0.89-1.78 mM). Urate-2-(14)C recovery was almost complete and there was no delayed excretion, demonstrating saturation kinetics. These findings are compatible with a carrier-mediated mechanism for urate transport probably located at the luminal border of the proximal tubular epithelium. No definitive evidence for urate secretion was found in these studies.

Aminohippuric Acids↗