Angiotensin II receptor density in the brain is elevated when dietary salt intake is raised or in the state of hypertension. The aim of this study was to evaluate whether the angiotensin II modulation of the baroreceptor control of renal sympathetic nerve activity was altered under these conditions. Wistar rats, fed either a regular (0.25% w/w sodium) or high-salt diet (3.1% w/w sodium), or stroke-prone spontaneously hypertensive rats (SHRSPs) were implanted with cannulae in the carotid artery, jugular vein and the cerebroventricle and with recording electrodes on the renal sympathetic nerves. Three days later, baroreceptor gain curves were generated for renal sympathetic nerve activity and heart rate before and following intracerebroventricular (I.C.V.) administration of losartan (15 μg) to block angiotensin AT1 receptors. The rats fed a regular diet had a mean blood pressure of 116 ± 3 mmHg and heart rate of 467 ± 25 beats min −1 , which remained unchanged after the I.C.V. administration of losartan. The sensitivity or curvature coefficient of the baroreceptor curve for renal sympathetic nerve activity was increased by 36% (P < 0.05) following losartan. In the rats fed a high-salt diet, all cardiovascular variables and the losartan-induced increase in the baroreceptor curvature coefficient for renal sympathetic nerve activity (29%) were similar to values in rats on the regular sodium diet. The heart rate baroreceptor curvature coefficient was not altered in either the rats fed a regular or a high-salt diet. The slope of the renal sympathetic nerve activity baroreflex gain curve in the SHRSPs was less and the increase following administration of losartan (54%) was greater than in the Wistar rats. These data indicate that in the conscious state, the tonic inhibitory action of brain angiotensin II on the baroreflex regulation of renal sympathetic nerve activity was unaffected by raised dietary sodium, but its role was enhanced in the SHRSPs.

This investigation examined the renal sympathetic nerve and renal excretory responses to somatosensory stimulation in normotensive and stroke-prone spontaneously hypertensive rats (SHRSP). Somatosensory activation was achieved by either subcutaneous capsaicin administration or exposure of the airways tract to irritant fumes from acetic acid in chloralose-urethan-anesthetized animals. In Wistar rats, blood pressure increased between 10 and 20% ( P < 0.001–0.01), renal perfusion pressure was maintained unchanged, renal hemodynamics were unaltered, and urine flow and sodium excretion were decreased by 25 to 50% ( P < 0.001–0.05). In the SHRSP, the somatosensory-induced increases in blood pressure were slightly larger (∼15–20% P < 0.05) than those of the Wistar rats, whereas the excretory responses were one-half those of the normotensive animals ( P < 0.05). The somatosensory challenges reflexly increased integrated renal sympathetic nerve activity in both normotensive and hypertensive rats. The power spectral analysis demonstrated that the increases in percentage power at heart rate frequency and total power were two to three times more ( P < 0.05) in the Wistar rats compared with the SHRSP. The reduced ability of the SHRSP to modulate the energy in the renal sympathetic nerve signal at heart rate frequency might explain in part the attenuated functional responses to the somatosensory challenges.

This study examined the renal nerve-dependent renal hemodynamic and tubular responses to somatosensory stimulation in the anesthetized rat by use of subcutaneously applied capsaicin when the action of ANG II was blocked peripherally or selectively within the brain. Activation of skin somatosensory receptors caused a transient reversible 10–15% increase in blood pressure, and while renal perfusion pressure was regulated at control levels, there was a transient fall in urine flow and sodium excretion even though both renal blood flow and glomerular filtration rate were unchanged. These reflexly induced excretory responses were abolished when the renal nerves were sectioned. Administration of the ANG II AT1-receptor antagonist, losartan, either intravenously at 3 or 10 mg/kg or locally into the lateral cerebroventricles at 15 μg plus 7.5 μg/h, had no effect on capsaicin-induced vasopressor responses but blocked the reductions in urine flow and sodium excretion. These findings are consistent with ANG II being involved in at least two stages in the reflex, one centrally and one at the periphery.

The data show that both the ET(A)/ET(B) and selective ET(A)-receptor antagonist ameliorated the ischaemia-reperfusion injury when given in the peri-ischaemic period but not when the ET(A)-receptor antagonist was given for 60 min at 100 micro g/kg/min after the ischaemic period.

1 This investigation examined the autoregulatory efficiency of different vascular regions of the normotensive and stroke prone-spontaneously hypertensive rat (SP-SHR) kidney and determined how these myogenic responses were dependent upon extracellular calcium. In acute studies, renal autoregulatory blood perfusion curves for cortex and papilla were generated, autoregulatory indices (Al's) calculated as a ratio of the perfusion change divided by the ratio of the pressure difference where zero represents perfect and 1 equates to no autoregulation. The influence of a calcium channel antagonist on this Al was measured at both cortex and papilla. 2 Rats were anaesthetized with sodium pentobarbitone, the kidney exposed and cortical and papillary perfusion measured by Laser-Doppler flowmetry. Groups of rats either received no drug or nitrendipine at either 0.125 or 0.25 fig kg-' min-'. 3 In the Wistar normotensive rats there was efficient autoregulation in the cortex (AI = 0.21 ± 0.17), from 127 to 90 mmHg, but not in the papilla (Al = 0.89 ± 0.08), while below 90 mmHg perfusion in both regions decreased with renal perfusion pressure. Nitrendipine attenuated cortical autoregulation at the higher pressure range (AI = 0.62 ± 0.13 and 0.92 ± 0.10 at the low and high dose, respectively) while having no effect on the papillary pressure perfusion pattern. 4 In the SP-SHR, reduction in renal perfusion pressure, from 150 to 100 mmHg, gave a cortical Al of 0.49 ± 0.10, indicating impaired autoregulation, whereas the papilla demonstrated little myogenic response. Over the high pressure range in the presence of both doses of nitrendipine there was neither cortical (Al of 0.75 ± 0.11 and 0.94 ± 0.12, respectively) nor papillary autoregulation. 5 Autoregulation in the renal cortex but not papilla of the young Wistar rats is well developed. The myogenic responses are attenuated by the calcium channel antagonists suggesting that they are dependent upon the availability of extracellular calcium. Cortical autoregulation in the SP-SHR is deficient compared to the normotensive rats and is further impaired by the calcium channel antagonists.