The present study was designed to test the hypothesis that during whole body heating (WBH), nitric oxide (NO) synthesized in the endothelium acts synergistically with an unknown neurotransmitter to elicit active vasodilation. Rabbits were instrumented for the measurement of mean arterial pressure, heart rate, and ear blood flow (EBF) (Doppler ultrasound). During WBH, either N omega-nitro-L-arginine methyl ester (L-NAME, 10-40 mg over 10-15 min, n = 6 rabbits; group 1), a NO synthase inhibitor, or saponin (30-40 mg over 10-20 min, n = 6 rabbits; group 2), a detergent that denudes the endothelium, was given via a lingual artery catheter until thermoregulatory vasodilation was reversed. When EBF stabilized at the new reduced level, the NO donor, sodium nitroprusside (SNP), was infused (0.2-1.0 mg/ml, 0.01-0.05 ml/min, 2-5 min) via the lingual artery catheter. During WBH, EBF increased from 0.39 +/- 0.08 to 6.47 +/- 0.63 kHz in group 1, and from 0.69 +/- 0.18 to 5.72 +/- 0.49 kHz in group 2. Infusion of L-NAME decreased EBF in group 1 to 1.97 +/- 0.40 kHz. Infusion of saponin decreased EBF in group 2 to 1.23 +/- 0.40 kHz. Subsequent SNP infusion during hyperthermia returned EBF to 6.88 +/- 0.72 kHz in group 1 and 5.53 +/- 1.27 kHz in group 2 but had no effect when administered during normothermia. These results suggest that NO acts in conjunction with another substance, presumably the neurotransmitter released on WBH, to elicit thermoregulatory vasodilation.
The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.
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This study investigated the effect of chemical and electrical stimulation of the area postrema on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in urethan-anesthetized rabbits. Electrical stimulation of the area postrema at 2, 5, 10, 20, 40, and 80 Hz using constant currents of 7.5, 15, and 30 microA (pulse duration = 0.3 ms, train duration = 5 s) produced progressive decreases in RSNA and heart rate, with no consistent change in arterial pressure. To control for electrical activation of fibers of passage in or near the area postrema, L-glutamate was injected into the area postrema using glass micropipettes. Micropressure injection of L-glutamate (10 mM) in volumes of 5-10 nl produced rapid decreases in RSNA averaging 27 +/- 5% (P less than 0.05) accompanied by a small bradycardia. The effects of electrical stimulation of the area postrema, but not the adjacent nucleus tractus solitarius, were totally eliminated by micropressure injection of kainic acid (40 ng in 40 nl) into the area postrema. During continuous electrical stimulation of the area postrema using parameters that produced small decrements in RSNA and heart rate, the slope of the line relating baroreflex inhibition of RSNA to increases in arterial pressure during graded infusions of phenylephrine was significantly enhanced (-6.77 +/- 1.30 vs. -3.81 +/- 0.66% RSNA/mmHg). These data are consistent with the hypothesis that activation of neurons in the area postrema results in an inhibition of RSNA. Furthermore, stimulation of the area postrema augments baroreflex inhibition of RSNA during increases in arterial pressure with phenylephrine.
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