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Viscoelastic and electrophysiological mechanisms have been implicated in the resetting of baroreceptors in hypertension, but resetting in response to hypotension has been less studied. To evaluate the temporal relationship between viscoelastic mechanisms and acute resetting, we examined the "in vivo" behavior of aortic caliber and aortic baroreceptor activity during step changes in pressure. Fifteen-minute hemorrhage in Wistar rats produced stable hypotension (30 mmHg) and viscoelastic contraction (111 +/- 14.2 microns systolic caliber; P < 0.01). Integrated aortic activity fell to 19.8 +/- 3.9% of control (P < 0.001) after 3 s of hypotension but recovered to 64 +/- 4.1% 15 min later (P < 0.01 from 3 s). Recovery of baroreceptor activity was linearly correlated to viscoelastic contraction (r = 0.963; P < 0.0001). Thirty-minute phenylephrine infusion (1.0-4.0 micrograms/min) produced stable hypertension (30 mmHg) and viscoelastic dilation (211 +/- 37.0 microns systolic caliber). Integrated aortic activity increased to 218.0 +/- 18% of control values (P < 0.001) 30 s after hypertension and was reduced to 164.0 +/- 12.0% (P < 0.001 from 3 s) within 30 min. Reduction of baroreceptor activity correlated linearly with viscoelastic relaxation (r = 0.963; P < 0.0001). The results indicate that in the in vivo rat aorta, viscoelastic mechanisms parallel and may contribute to the baroreceptor resetting during hypotension and hypertension.

The aging process is associated with alterations in the autonomic control of cardiovascular function. In the present study, we observed that reflex bradycardia and tachycardia produced by pressor and depressor agents were attenuated in old (24 mo) rats [70 and 56% of responses in young rats (4 mo), respectively]. In contrast, the bradycardia induced by chemoreflex activation with increasing doses of KCN (60, 100, 140, and 180 micrograms/kg) was greater in old [-30 +/- 19, -155 +/- 32, -198 +/- 15, and -204 +/- 24 beats/ min (bpm)] than in young rats [-13 +/- 6, -75 +/- 20 (P < 0.05), -99 +/- 26 (P < 0.05), and -103 +/- 20 (P < 0.05) bpm]. The chemoreflex-pressor responses tended to be greater in old (12 +/- 6, 47 +/- 6, 54 +/- 7, and 55 +/- 5 mmHg) than in young rats (4 +/- 2, 32 +/- 8, 42 +/- 6, and 44 +/- 4 mmHg), but the differences between both groups were not statistically significant. However, pressor responses were higher in old rats after the chemoreflex-activated bradycardia was attenuated by atropine (4 mg/kg iv) [old (17 +/- 9(1) P < 0.05; 57 +/- 4, P < 0.05; 61 +/- 4; and 64 +/- 5 mmHg) vs. young (3 +/- 2, 29 +/- 9(1) 50 +/- 5, and 58 +/- 7 mmHg)]. Administration of the alpha 1-blocker prazosin (1 mg/kg iv) blunted pressor responses but did not change the bradycardia induced by chemoreflex in both groups. In conclusion, our data indicate that the bradycardia and pressor responses to chemoreflex activation were exaggerated, whereas the heart rate responses (bradycardia and tachycardia) to baroreflex were depressed in old rats.

The effect of exercise training (ET) on renal sympathetic nerve activity (RSNA), baroreflex control of RSNA and heart rate (HR), and arterial pressure (AP) responsiveness to phenylephrine and angiotensin II (ANG II) was studied in six trained (T) and six sedentary (S) male Wistar rats. ET was performed on a motor treadmill for 13 wk. The RSNA signals of unanesthetized rats were processed by an analog-to-digital converter to quantify the nerve discharges associated with changes in AP and HR. The reflex control of RSNA and HR were evaluated during progressive injections of phenylephrine and sodium nitroprusside. Mean arterial pressure (MAP) was similar in both groups. RSNA was significantly lower in T rats (28 +/- 2 vs. 36 +/- 3%). T rats had an impairment of baroreflex control of RSNA in response to nitroprusside (4.9 +/- 0.89 vs. 12.3 +/- 1.2 bars.cycle-1.mmHg-1). ET decreased AP responsiveness for phenylephrine and ANG II. Therefore ET produces 1) no change in resting MAP but a significant decrease in RSNA and AP responsiveness and 2) partial impairment of baroreflexes, i.e., bradycardic responses and RSNA during MAP decrease.

Rapid or acute resetting of the aortic baroreceptors was studied in anesthetized rats during the onset and maintenance of hypertension produced by subdiaphragmatic aortic constriction for up to 6 h. After 2 min of hypertension, the systolic threshold pressure for activation of the baroreceptors increased by 33% of the total 27-mmHg increase of the control diastolic pressure. Maximal resetting of 46 and 52% was demonstrable after 20 and 30 min of hypertension. The shifts in pressure threshold were accompanied by parallel shifts in the entire baroreceptor function curves. After 30 min of hypertension, resetting was only partially (60%) reversed within the 30 min of pressure normalization. Resetting did not progress with time. Six hours after aortic constriction, resetting was only 38% (vs. 32% after 30 min). The data indicate that acute or rapid resetting of the aortic baroreceptors reaches a maximum within 20-30 min (40-50%) and remains stable for up to 6 h, with no apparent change in the baroreceptor gain.