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Biomedical subjects

Geoffrey A Head

Publications and source records attributed to Geoffrey A Head.

23 records · Page 2Linked to original sources

Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits.

In this study, we examined the effect of excitatory amino acid (EAA) receptor blockade in the rostral ventrolateral medulla (RVLM) on the renal sympathetic baroreflex in conscious rabbits. Rabbits were implanted with guide cannulas for bilateral microinjections into the RVLM (+2 to +3 mm from the obex, n = 8) or into the intermediate ventrolateral medulla (IVLM; 0 to +1 mm from the obex, n = 5) and with an electrode for measuring renal sympathetic nerve activity (RSNA). After 7 days of recovery, microinjection of the EAA receptor antagonist kynurenate (10 nmol) into the RVLM did not affect resting RSNA or arterial pressure. Kynurenate decreased the gain of the RSNA baroreflex by 53% but did not change the reflex range. By contrast, injection of kynurenate into the IVLM increased resting arterial pressure and RSNA by 27 mmHg and 88%, respectively, but did not alter the RSNA baroreflex gain or range. Pentobarbital sodium anesthesia attenuated the gain and range of the RSNA baroreflex by 78 and 40%, respectively. Under these conditions, microinjection of kynurenate into the RVLM did not cause any further change in the gain of this reflex. These results suggest that endogenous EAA neurotransmitters in the RVLM are important in modulating the sympathetic baroreflex in conscious rabbits. Anesthesia can mask the functional significance of EAAs in the RVLM in modulating the baroreflexes, which may explain why previous studies in anesthetized animals found no effect of blocking EAA receptors in the RVLM on sympathetic baroreflexes.

Animals↗

Ionotropic glutamate receptors in the rostral ventrolateral medulla mediate sympathetic responses to acute stress in conscious rabbits.

In conscious, chronically instrumented rabbits (n = 7), airjet stress evoked increases in arterial pressure (AP) and renal sympathetic nerve activity (RSNA), which were greatest in the first 2 min (+ 10 mm Hg and + 127%, respectively), but then rapidly reached a stable level (+ 7 mm Hg and + 37%, respectively). Bilateral microinjection into the rostral ventrolateral medulla (RVLM) of an ionotropic excitatory amino acid (EAA) receptor antagonist kynurenate (10 nmol/200 nl) did not affect resting AP and RSNA, but reduced their initial peak responses to airjet by 80% and 52%, respectively, without altering the stable levels of these responses. By contrast, bilateral microinfusion of glutamate (2 nmol/20 nl/min) into the RVLM increased resting AP by 13 mm Hg, but did not alter the RSNA and AP responses to airjet stress. These results suggest that the RVLM is an essential site for conveying excitatory environmental influences to the sympathetic nervous system in conscious rabbits. The EAA receptors are critically important in initiating the pressor and sympathoexcitatory responses to acute emotional stress, but play relatively little role in the maintenance of these responses.

Acute Disease↗

A real-time algorithm for the quantification of blood pressure waveforms.

A real-time algorithm for quantification of biological oscillatory signals, such as arterial blood pressure (BP) is proposed which does not require user intervention and works on waveforms complicated by rapid changes in the mean level, frequency, or by the presence of arrhythmia. The algorithm is based on the continous independent assessment of the refractory period (RP). In the first stage, a sample of the signal is band-pass filtered. During the next stage: 1) the local maxima in the filtered signal are identified and their pulse amplitudes (PA) measured on the side opposite to the possible notch position and 2) those maxima whose PA exceeds some threshold are selected and an array of RP values is formed as a fraction of the moving estimate of the interval between successive selected peaks. Finally, the original signal is analyzed by means of two moving averages (MAs) with short and long averaging time intervals. The true peaks are determined as the maxima between intersections of MAs if the peak-to-peak or the intersection-to-intersection intervals since the previous peak and the previous intersection exceed the RP. The algorithm proved to be superior against three commercially available heartbeat detectors yielding an error rate of 0.09%.

Algorithms↗

Sympathetic modulation of renal blood flow by rilmenidine and captopril: central vs. peripheral effects.

Renal blood flow (RBF) is modulated by renal sympathetic nerve activity (RSNA). However, agents that are supposed to reduce sympathetic tone, such as rilmenidine and captopril, influence RBF also by direct arteriolar effects. The present study was designed to test to what extent the renal nerves contribute to the renal hemodynamic response to rilmenidine and captopril. We used a technique that allows simultaneous recording of RBF and RSNA to the same kidney in conscious rabbits. We compared the dose-dependent effects of rilmenidine (0.01-1 mg/kg) and captopril (0.03-3 mg/kg) on RBF and RSNA in intact and renal denervated (RNX) rabbits. Because rilmenidine and captopril lower blood pressure, studies were also performed in sinoaortically denervated (SAD) rabbits to determine the role of the baroreflex in the renal hemodynamic response. Rilmenidine reduced arterial pressure, RBF, and RSNA dose dependently. In intact rabbits (n = 10), renal conductance (RC) remained unaltered (3 +/- 5%), even after the 1-mg/kg dose, which completely abolished RSNA. In RNX rabbits (n = 6), RC fell by 18 +/- 5%, whereas in SAD rabbits (n = 7) RC increased by 30 +/- 20% after rilmenidine. In intact rabbits, captopril increased RSNA maximally by 64 +/- 8%. RSNA did not rise in SAD rabbits. Despite the differential response or absence of RSNA, captopril increased RC to a comparable degree (maximally 40-50%) in all three groups. Using spectral analysis techniques, we found that in all groups, independently of ongoing RSNA, captopril, but not rilmenidine, attenuated both myogenic (0.07-0.25 Hz) and tubuloglomerular feedback (0.01-0.07 Hz) related fluctuations in RC. We conclude that, in conscious rabbits, the renal vasodilator effect of rilmenidine depends on the level of ongoing RSNA. Its sympatholytic effect is, however, blunted by a direct arteriolar vasoconstrictor effect. In contrast, the renal vasodilator effect of captopril is not modulated by ongoing RSNA and is associated with impairment of autoregulation of RBF.

Animals↗