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Biomedical subjects

U C Kopp

Publications and source records attributed to U C Kopp.

42 records · Page 3Linked to original sources
PubMed1985

Modulation of reflex renal vasoconstriction by increased endogenous renal prostaglandin synthesis.

The effect of increased endogenous renal prostaglandin synthesis on the reflex renal vasoconstrictor response to stimulation of skeletal muscle somatic receptors and their afferents was examined in anesthetized dogs with bilateral carotid artery occlusion and vagotomy. Acute ureteral occlusion and indomethacin were used to acutely increase and decrease, respectively, endogenous renal prostaglandin synthesis. Graded electrical stimulation of the afferent sciatic nerve or antegrade femoral arterial injection of capsaicin elicited a frequency dependent reduction in renal blood flow accompanied by increases in mean arterial pressure and heart rate. Acute ureteral occlusion attenuated (circa 50%) the renal vasoconstrictor response but did not affect the increases in mean arterial pressure or heart rate. Administration of indomethacin during continued ureteral occlusion restored the renal vasoconstrictor responses to the preureteral occlusion level. These results indicate that the increase in endogenous renal prostaglandin synthesis during acute ureteral occlusion specifically attenuates the reflex renal vasoconstrictor response to stimulation of skeletal muscle somatic receptors and their afferents.

Animals↗
PubMed1984

Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat.

The renal functional effects of renal mechano- (MR) and chemoreceptor (CR) stimulation were examined in dogs and rats. In dogs increasing ureteral pressure (increases UP) increased ipsilateral (ipsi) renal blood flow and renin secretion rate, decreased contralateral (contra) renal blood flow, but did not affect contra renal excretion or renin secretion rate. Increasing renal venous pressure (increases RVP) increased ipsi renin secretion rate but did not affect contra renal function. Retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect either ipsi or contra renal function. In rats,increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect mean arterial pressure, heart rate, contra renal blood flow, or glomerular filtration rate but increased contra urine flow rate and urinary sodium excretion. Increasing ureteral pressure with 0.1 M NaCl increased contra urine flow rate and urinary sodium excretion, whereas retrograde ureteropelvic perfusion with 0.1 M NaCl was without effect. Thus increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl stimulated renal MR and CR, respectively. The contra diuretic and natriuretic responses to renal MR and CR stimulation were abolished by either ipsi or contra renal denervation. Renal MR and CR stimulation increased ipsi afferent renal nerve activity (RNA) and decreased contra efferent RNA. These results indicate that in dogs renal MR stimulation results in a modest contralateral excitatory renorenal reflex, whereas in rats renal MR and CR stimulation produce a contralateral inhibitory renorenal reflex.

Animals↗
PubMed1984

Interaction between neural and nonneural mechanisms controlling renin secretion rate.

The interaction between the neural and nonneural mechanisms in the control of renin secretion rate was studied in anesthetized vagotomized dogs at renal arterial pressures of 170, 130, 90, and 50 mmHg. Left renal nerves were stimulated (RNS) at either 0.075, 0.3, or 0.7 Hz and the right kidney was denervated. At spontaneous renal arterial pressure RNS at 0.075, 0.3, and 0.7 Hz decreased renal blood flow 0, 1 +/- 0, and 2 +/- 1%, respectively, and urinary sodium excretion 0, 2 +/- 1, and 22 +/- 3%, respectively. RNS at 0.075 Hz augmented renin secretion rate at 50 mmHg by 1,806 +/- 505 ng/min; there was no augmentation at 90, 130, and 170 mmHg. RNS at 0.3 Hz augmented renin secretion rate at 50 and 90 mmHg by 2,635 +/- 824 and 1,197 +/- 289 ng/min, respectively; there was no augmentation at 130 and 170 mmHg. RNS at 0.7 Hz augmented renin secretion rate at 50, 90, and 130 mmHg by 1,421 +/- 287, 747 +/- 172, and 273 +/- 163 ng/min, respectively; there was no augmentation at 170 mmHg. RNS at 0.075 Hz to one kidney and 0.7 Hz to the other kidney in the same dog demonstrated that the renin secretion rate was greater with RNS at 0.7 Hz than with 0.075 Hz at 50 and 90 mmHg but not at 130 and 170 mmHg. We conclude that the nonneural and neural mechanisms interact in the control of renin secretion rate. The degree of interaction depends on the level of renal arterial pressure and the intensity of RNS.

Animals↗
PubMed1984

Interactions among renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin release.

To examine the interactions among the renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin secretion, experiments using low-frequency renal nerve stimulation (LFRNS; supramaximal voltage, 0.5 ms, 0.5 Hz) were performed in anesthetized dogs. LFRNS, which did not affect renal hemodynamics or urinary sodium excretion, increased renin secretion rate before (79 +/- 16 ng/min) but significantly less after renal arterial administration of indomethacin or meclofenamate (26 +/- 7 ng/min). In a separate group of dogs, LFRNS increased both renin secretion rate (266 +/- 139 ng/min) and renal prostaglandin E2 secretion rate (2,080 +/- 635 ng/min). LFRNS does not alter input stimuli to the renal vascular baroreceptor or tubular macula densa receptor mechanisms for renin secretion and represents a direct neural stimulus for renin secretion; this also increases renal prostaglandin E2 secretion rate, which contributes to the increase in renin secretion rate. The renin secretion rate response of innervated and denervated kidneys to reduction in renal arterial pressure to 50 mmHg was examined before and after indomethacin/meclofenamate administration. The observation that indomethacin/meclofenamate decreased but did not abolish the renin secretion rate response to aortic constriction in innervated kidneys suggests the presence of a prostaglandin-independent mechanism that is mediated by an interaction between the renal nerves and the tubular macula densa receptor, as indomethacin/meclofenamate essentially abolished the renin secretion rate response to aortic constriction in denervated kidneys.

Animals↗
PubMed1983

Effects of physiological increments in renal arterial plasma osmolality on renin secretion rate.

The present study was performed in anesthetized dogs to examine the effects of physiological increments in renal arterial plasma osmolality on basal renin secretion rate and on the response of renin secretion rate to RNS. Three concentrations of hypertonic NaCl were infused into the renal artery (i.r.a.) at 0.38 ml/min for 3 min; i.r.a. Hypertonic NaCl at 0.45M, 0.9M, and 1.8M increased the renal arterial plasma osmolality by 6 +/- 2, 8 +/- 2, and 28 +/- 9 mOsm/kg H2O, respectively. NaCl, 0.45M, did not affect renal function, whereas both 0.9M and 1.8M NaCl increased renal blood flow and urinary sodium excretion; neither 0.45M, 0.9M, nor 1.8M NaCl affected renin secretion rate. RNS was applied at two different frequencies: LFRNS and HFRNS. LFRNS did not affect renal blood flow, whereas HFRNS reduced renal blood flow by 50%. Both LFRNS and HFRNS increased renin secretion rate significantly. An i.r.a. infusion of 0.9M NaCl increased urinary sodium excretion and reduced the renin secretion rate response to LFRNS (-52% +/- 15, p less than 0.02) and HFRNS (-25% +/- 8, p less than 0.01). These findings demonstrate that increases in renal arterial plasma osmolality within the physiological range increase renal blood flow but do not affect renal secretion rate. The renal secretion rate response to RNS is attenuated by increased renal arterial plasma osmolality, an effect consistent with increased sodium chloride delivery to the distal tubular macula densa receptor.

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