Abstract
Hypothermia-induced reduction of metabolic rate is accompanied by depression of both glomerular perfusion and filtration. The present study investigated whether these changes are linked to changes in renal autoregulation and nitric oxide (NO) signalling. During hypothermia, renal blood flow (RBF) and glomerular filtration rate (GFR) were reduced and urine production was increased, and this was linked with reduced plasma cGMP levels and increased renal vascular resistance. Although stimulation of NO production decreased vascular resistance, blood pressure and urine flow, intravenous infusion of the NO precursor L-arginine or the NO donor sodium nitroprusside did not alter RBF or GFR. In contrast, inhibition of NO synthesis by Nw-nitro-L-arginine led to a further decline in both parameters. Functional renal autoregulation was apparent at both temperatures. Below the autoregulatory range, RBF in both cases increased in proportion to the perfusion ±pressure, although, the slope of the first ascending limb of the pressure-flow relationship was lower during hypothermia. The main difference was rather that the curves obtained during hypothermia levelled off already at a RBF of 3.9 ± 0.3 mL/min then remained stable throughout the autoregulatory pressure range, compared to 7.6 ± 0.3 mL/min during normothermia. This was found to be due to a threefold increase in, primarily, the afferent arteriolar resistance from 2.6 to 7.5 mmHg min mL−1. Infusion of sodium nitroprusside did not significantly affect RBF during hypothermia, although a small increase at pressures below the autoregulatory range was observed. In conclusion, cold-induced rise in renal vascular resistance results from afferent arteriolar vasoconstriction by the autoregulatory mechanism, setting RBF and GFR in proportion to the metabolic rate, which cannot be explained by reduced NO production alone.
Highlights
In our previous studies [5, 6], moderate hypothermia at 28 °C (HT) was found to be accompanied by an approximately 50% reduction of total renal blood flow (RBF), and glomerular filtration rate (GFR) compared with normothermia (NT) at 37.5 °C
In the second hypothermic period, the vascular resistance remained essentially unchanged after intravenous infusion of either the nitric oxide (NO) precursor Larginine or the NO donor sodium nitroprusside (SNP)
The same pattern was observed in normothermia (Table 2), where L-arginine and SNP only evoked modest changes in renal vascular resistance (RVR)
Summary
In our previous studies [5, 6], moderate hypothermia at 28 °C (HT) was found to be accompanied by an approximately 50% reduction of total renal blood flow (RBF), and glomerular filtration rate (GFR) compared with normothermia (NT) at 37.5 °C. Since the blood pressure remained largely unchanged, it was calculated that the renal vascular resistance increased twofold, of which 75% was attributed to active vasoconstriction of, primarily, the afferent arteriole. In search for the factor(s) underlying this pronounced vasoconstriction, an activation of the sympathetic nervous system, our major cold defence system [17], was an unlikely candidate since direct recordings showed that efferent renal sympathetic nerve activity was decreased [6, 30, 33]. A study using micropuncture technique showed that both single nephron GFR, and proximal and distal tubular fluid flow decreased by approximately. The diuresis, increased three- to sixfold that could be attributed to a vasopressin-dependent decrease in water reabsorption at the distal tubule and collecting duct [7]
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