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Biomedical subjects

E D Moreira

Publications and source records attributed to E D Moreira.

At least 37 records · Page 2Linked to original sources
PubMed1998

Chronic AT1 receptor blockade alters aortic nerve activity in hypertension.

In the chronic phase of coarctation hypertension (CH) we have shown both reduction in baroreceptor sensitivity (Hypertension. 1992;19[suppl II]:II-198-II-201.) and normalization of the depressed baroreceptor reflex control of heart rate, even with the persistence of hypertension in losartan-treated animals (Am J Physiol. 1995;269:H812-H818). In the present study we analyzed the effects of angiotensin II blockade on afferent aortic nerve activity of CH and sham-operated groups treated chronically with vehicle or losartan (10 mg/kg per day p.o.). CH was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 8 days (4 control and 4 experimental days). Aortic pressure (conscious rats) and aortic nerve activity simultaneous to pressure (anesthetized rats) were recorded on the fourth day of the experimental period. Losartan-treated rats showed reduced tail pressure (104+/-3 versus 117+/-3 mm Hg in the vehicle group). In both groups, aortic coarctation caused a significant increase in pressure (25% and 28%, respectively) and a depression of the aortic nerve activity/pressure relationship when compared with sham-operated coarcted animals. In the physiological range of pressure changes, the depression was significantly smaller after losartan treatment (3.30+/-0.33 versus 2.18+/-0.37%/mm Hg in the losartan- and vehicle-treated CH groups, respectively, versus 5.05+/-0.33%/mm Hg in the sham-operated vehicle-treated group). Angiotensin type 1 (AT1) receptor blockade was also accompanied by reduced variability of the afferent discharge. The data suggested that apart from its pressure effect, angiotensin II acts at AT1 receptors to decrease the sensitivity of aortic afferents during physiological (+/-10 mm Hg) increases and decreases in pressure. Thus, angiotensin II may contribute to reductions of baroreceptor gain in chronic hypertension.

Afferent Pathways↗
PubMed1996

Viscoelastic mechanisms of aortic baroreceptor resetting to hypotension and to hypertension.

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.

Animals↗
PubMed1996

Alterations in the cardiovascular control by the chemoreflex and the baroreflex in old rats.

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.

Aging↗
PubMed1995

Changes of renal sympathetic activity in acute and chronic conscious sinoaortic denervated rats.

The arterial pressure level attained in sinoaortic denervated rats depends on the net effect of eliminating excitatory and inhibitory influences (chemoreceptor and baroreceptor elimination, respectively). After sinoaortic denervation is completed, the hypertension usually observed within the first few days is followed by normotension at the chronic stages. In this work renal sympathetic nerve activity was measured in conscious, unrestrained rats 6 hours (acute) and 20 days (chronic) after sinoaortic denervation. Increased arterial pressure (154 +/- 10 versus 114 +/- 3 mm Hg in controls) and renal sympathetic nerve activity (32 +/- 5 versus 13 +/- 2 bars per cycle in controls) with no changes in heart rate (404 +/- 17 vs 380 +/- 26 beats per minute) were observed in rats with acute sinoaortic denervation. In rats with chronic sinoaortic denervation, arterial pressure (119 +/- 8 mm Hg) and renal sympathetic nerve activity (13 +/- 6 bars per cycle) returned to control levels. Bradycardiac and tachycardiac responses to changes in blood pressure were reduced to 88% and 89%, respectively, in rats with acute sinoaortic denervation and 76% and 74%, respectively, in rats with chronic sinoaortic denervation. The reflex control of renal sympathetic nerve activity after acute and chronic sinoaortic denervation showed an impairment of sympathoinhibition (0.13 +/- 0.02 and 0.25 +/- 0.1 bars per cycle, respectively, versus 0.9 +/- 0.17 bars per cycle in controls). Sympathoexcitatory responses also were impaired in rats with acute and chronic sinoaortic denervation (0.08 +/- 0.03 and 0.37 +/- 0.1 bars per cycle, respectively, compared with 0.98 +/- 0.2 bars per cycle in controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

DuP 753 is more effective than captopril on baroreceptor function in high-renin hypertension.

High-renin hypertensive rats exhibit a general impairment of the baroreceptor reflexes. In the present study we compared the effect of the angiotensin converting enzyme inhibitor captopril (10 mg/kg per day) with the effect of the selective angiotensin subtype 1 receptor blocker DuP 753 (10 mg/kg per day) on the baroreceptor reflex bradycardia (progressive doses of phenylephrine) and baroreceptor reflex tachycardia (progressive doses of nitroprusside) in conscious rats 7 days after aortic ligation. Arterial pressure was markedly reduced after both acute (15-minute) treatment with captopril (123 +/- 6 versus 184 +/- 23 mm Hg) and DuP 753 (140 +/- 10.5 versus 181 +/- 5.4 mm Hg), but the depressed baroreceptor reflex bradycardia increased only after DuP 753 (1.13 +/- 0.22 versus 0.75 +/- 0.60 beats per minute [bpm]/mm Hg) and remained attenuated after captopril (0.54 +/- 0.086 versus 0.30 +/- 0.07 bpm/mm Hg). After a 2-day treatment, captopril reduced arterial pressure (95 +/- 5 versus 184 +/- 2.3 mm Hg) to lower levels than DuP 753 (119 +/- 6 versus 172 +/- 4.6 mm Hg), whereas the depressed baroreceptor reflex bradycardia remained unchanged with captopril (0.46 +/- 0.13 versus 0.31 +/- 0.076 bpm/mm Hg) and increased with DuP 753 (1.13 +/- 0.19 versus 0.38 +/- 0.12 bpm/mm Hg). Neither DuP 753 nor captopril administered acutely (15 minutes) or for 2 days significantly altered the depressed baroreceptor reflex tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1993

Effect of exercise training on RSNA, baroreflex control, and blood pressure responsiveness.

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.

Angiotensin II↗
PubMed1993

Seroepidemiology of human T-cell lymphotropic virus type I/II in northeastern Brazil.

We investigated the prevalence of human T-lymphotropic virus I/II (HTLV-I/II) infection in Bahia, a state in Northeastern Brazil. Healthy individuals (n = 327) and patients (n = 337) with a variety of diseases were screened for antibodies to HTLV-I/II using an enzyme immunoassay and Western blot. The overall prevalence among healthy subjects was 1.8% (six of 327); among patients it was 18.4% (62 of 337). Patients with AIDS had the highest prevalence of HTLV-I/II infection, 22.7% (20/88), followed by randomly selected patients from an infectious disease hospital, 19.4% (25 of 129), and tuberculosis patients, 11.1% (10 of 90). Four of 14 patients with myelopathy and three of 16 patients with lymphoid leukemia or lymphoma were seropositive for HTLV-I/II. Sixty-three of 68 HTLV-I/II-positive specimens were then typed: 53 patients were HTLV-I positive, three patients were HTLV-II positive, and in seven patients the assay could not distinguish infection by HTLV-I or II. The finding among HIV-seropositive intravenous drug users in Bahia of coinfection with HTLV-I is contrasted with reports from other areas in which dual infection occurs with HTLV-II. Although high prevalence of HTLV-I infection was found in Bahia, the extent and clinical manifestations of HTLV-I/II infection in Brazil remains imprecisely defined, and further studies are needed.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Serologic validation of HIV infection in a tropical area.

We have defined human immunodeficiency virus type 1 (HIV-1) serologic reactivity in Brazilians living in an area endemic for tropical diseases. Enzyme-linked immunosorbent assay (ELISA) and Western blot (WB) analyses were performed on 342 patients with diseases including Chagas' disease, schistosomiasis, typhoid fever, helminthiasis, and cutaneous and visceral leishmaniasis. Nine percent of the visceral leishmaniasis patients' sera reacted in the HIV-1 ELISA but all were WB negative. All other sera from these patients were HIV negative. A total of 224 HIV-1 ELISA repeatedly positive sera also were HIV-1 WB tested. They were drawn from a total population of 19,230 individuals, including AIDS patients, blood donors, homosexual men, intravenous drug users, pregnant women, individuals with hemophiliac, and tuberculosis and sexually transmitted disease patients. The WB results were analyzed using five different interpretive criteria for WB positivity. The Centers for Disease Control (CDC) and the World Health Organization (WHO) criteria were the most sensitive and specific for identifying HIV-1-infected individuals. The WB pattern was similar to that seen in the United States. Envelope (ENV) protein antibodies were highly predictive of HIV-1 infection; none of the AIDS patients lacked ENV protein reactivity. We conclude that among the tropical diseases studied, only visceral leishmaniasis is associated with false-positive HIV-1 ELISA tests. Current CDC and WHO criteria for interpretation of HIV-1 WB tests are appropriate for Brazil.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Vagal function impairment after exercise training.

The present investigation was undertaken to evaluate the vagal function of trained (T) and sedentary (S) rats by use of different approaches in the same animal. After 13 wk of exercise training (treadmill for 1 h 5 times/wk at 26.8 m/min and 15% grade), T rats had a resting heart rate (HR) slightly but significantly lower than S rats (299 +/- 3 vs. 308 +/- 3 beats/min). T rats had marked reduction of the intrinsic HR (329 +/- 4 vs. 369 +/- 5 beats/min) after blockade by methylatropine and propranolol. They also exhibited depressed vagal and sympathetic tonus. Baroreflex bradycardia (phenylephrine injections) was reduced, bradycardic responses produced by electrical stimulation of the vagus were depressed, and responses to methacholine injection were decreased in T rats. Therefore several evidences of vagal function impairment were observed in T rats. The resting bradycardia after exercise training is more likely to be dependent on alterations of the pacemaker cells, inasmuch as the intrinsic HR was markedly reduced.

Animals↗
PubMed1992

Renal denervation normalizes pressure and baroreceptor reflex in high renin hypertension in conscious rats.

High renin hypertension is usually accompanied by impairment of the baroreceptor reflexes. This feature has been mostly ascribed to overactivity of the renin-angiotensin system. However, renal nerves could also modulate the baroreceptor reflexes. In the present experiments, the effect of renal denervation on the depressed baroreceptor reflexes was studied in rats subjected to aortic ligation between the renal arteries. Renal denervation of the ischemic kidney was performed at the same time as aortic ligation. The resulting effects on arterial pressure, heart rate, plasma renin activity, and baroreceptor reflex control of heart rate were studied 10-12 days after ligation and denervation. Aortic ligation induced high levels of mean arterial pressure (166 +/- 6 versus 110 +/- 3 mm Hg in controls), heart rate (380 +/- 9 versus 352 +/- 8 beats per minute in controls), and plasma renin activity (44 +/- 5 versus 6 +/- 1.2 ng angiotensin I/ml/hr). The baroreceptor reflex sensitivity for bradycardia and tachycardia was significantly reduced (-0.18 +/- 0.04 and -0.18 +/- 0.05, respectively, versus -2.3 +/- 0.01 and -2.4 +2- 0.1 beats per minute per mm Hg in controls). Denervation of the ischemic kidney attenuated the development of hypertension in aortic-ligated rats (122 +/- 3 mm Hg), lowering heart rate (319 +/- 8 beats per minute) and normalizing baroreceptor reflex sensitivity to bradycardia (-2.0 +/- 0.2 beats per minute per mm Hg) and to tachycardia (-4.0 +/- 0.1 beats per minute per mm Hg). Plasma renin activity was also normalized (4.3 +/- 2.4 ng angiotensin I/ml/hr).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Early depression of the baroreceptor sensitivity during onset of hypertension.

We studied the correlation of changes in gain sensitivity of the baroreceptors and the development of resetting of the baroreceptors 2 and 6 days after the onset of hypertension produced by subdiaphragmatic aortic constriction in rats. Mean arterial pressure of anesthetized rats was maintained at approximately the same level as that of conscious rats, and baroreceptor function curves were studied on a beat-to-beat basis by computer. After 2 days of hypertension, the difference between the systolic pressure threshold and the control diastolic pressure was -13 +/- 2 mm Hg (125 +/- 3 versus 138 +/- 4 mm Hg). Individual values showed that in seven of nine hypertensive rats, the difference was less than 15 mm Hg, indicating complete resetting. After 6 days of hypertension, all rats exhibited complete resetting, when the systolic pressure threshold was similar to control diastolic pressure (143 +/- 4 versus 141 +/- 2 mm Hg), indicating that more than 2 days of hypertension is necessary for full displacement of the pressure thresholds when all hypertensive rats are considered. Slopes of the baroreceptor curves after 2 and 6 days of hypertension showed that baroreceptor gain was depressed by 25% and 34%, respectively. The difference was not statistically significant (1.07 +/- 0.054% versus 0.94 +/- 0.049% and 1.43 +/- 0.075% in controls). When changes in pressure were circumscribed to a more physiological range, a depression of 25% in response to +10 mm Hg and 37% in response to -10 mm Hg was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Vagal and sympathetic control of heart rate during exercise by sedentary and exercise-trained rats.

1. The present investigation was undertaken to study the vagal and sympathetic effects of an acute bout of exercise on ten sedentary (S) and nine trained (T) rats. The exercise training was performed 5 times a week for 13 weeks on a motor treadmill, at 1.0 mph, 15% grade for 60 min. 2. Heart rate (HR) was recorded at rest and during exercise, 15% grade at 0.5, 0.8 and 1.0 mph, for 3 min per stage. Vagal and sympathetic effects were studied after the administration of methylatropine (3 mg/kg) and propranolol (4 mg/kg). 3. Exercise training significantly attenuated cardiac acceleration at 0.8 (441 +/- 8 vs 486 +/- 9 bpm in S, P < 0.05) and 1.0 mph (466 +/- 12 vs 508 +/- 6 bpm in S, P < 0.05). The vagal effect was significantly increased in the T group at 0.8 (72 +/- 5 vs 32 +/- 10 bpm in S, P < 0.05) and 1.0 mph (46 +/- 8 vs 15 +/- 7 bpm in S, P < 0.05). The sympathetic effect was significantly decreased in the T group at 0.8 (73 +/- 9 vs 112 +/- 9 bpm in S, P < 0.05) and 1.0 mph (96 +/- 11 vs 125 +/- 7 bpm in S, P < 0.05). The intrinsic HR behavior was not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The relationship between renal sympathetic nerve activity and arterial pressure after selective denervation of baroreceptors and chemoreceptors.

The relationship between an acute increase in arterial pressure and renal sympathetic nerve activity produced in rats under chloralose anesthesia after carotid and sinoaortic denervation was analyzed by quantifying the nerve activity associated with arterial pressure changes. After sinus denervation there was no change in arterial pressure (125 +/- 2.3 vs 124.6 +/- 5 mmHg, N = 6), but the renal sympathetic nerve activity (10.8 +/- 0.9 vs 8.0 +/- 1.1 bars s-1 cycle-1, N = 6) was significantly decreased. In spite of this, baroreflex control of renal sympathetic nerve activity was the same as during the control period. After sinoaortic denervation, there were simultaneous increases in arterial pressure (from 124 +/- 2.3 to 188 +/- 6 mmHg, N = 6) and renal sympathetic nerve activity (from 10.8 +/- 0.9 to 13.7 +/- 2.9 bars s-1 cycle-1) with marked attenuation of the baroreflexes. Spectral analysis of arterial blood pressure after sinus denervation showed a shift of a 1-Hz peak to 0.7 Hz, probably related to a decrease in respiratory frequency. The results suggest that after sinoaortic denervation the acute increase in arterial pressure is only due to aortic denervation.

Animals↗
PubMed1990

Rapid resetting of the baroreceptors in renal hypertensive rats.

The characteristics and extent of rapid or acute resetting of the aortic baroreceptors were studied in long-term renal hypertensive rats during 30 minutes of sustained hypertension produced by phenylephrine infusion. The aortic baroreceptors of hypertensive rats exhibited complete resetting to hypertension because during the control period the systolic threshold pressure for activation of the baroreceptors was similar (137 +/- 5 vs. 142 +/- 4 mm Hg) to the control diastolic pressure. Five minutes after onset of hypertension, a resetting of 32% (percent change of mean pressure threshold divided by total change of mean pressure) was demonstrable. The extent of resetting was 39%, 38%, and 41% after 10, 20, and 30 minutes of hypertension, respectively. When the percent change of systolic threshold pressure divided by total change of control diastolic pressure was used to calculate the extent of resetting, similar results were obtained. The extent of displacement of the entire baroreceptor pressure-response curves was similar to that of pressure thresholds. Reversibility of the resetting process was not complete within 30 minutes of pressure normalization after the administration of phenylephrine was interrupted. These data indicate that the characteristics and extent of rapid resetting of the baroreceptors of renal hypertensive rats, which were reset to operate at hypertensive levels, are similar to those previously described in normotensive rats.

Animals↗
PubMed1990

Reversibility of baroreceptor hyposensitivity during reversal of hypertension.

The extent and characteristics of reversal of baroreceptor resetting after pressure normalization were studied in rats with renal hypertension of 2 months' duration. During the control period, the displacement of the entire baroreceptor function curve was accompanied by a decrease slope, indicating that the gain sensitivity was depressed by 36% in the renal hypertensive rats. In response to changes of +10 and -10 mm Hg in the control pressure, the gain sensitivity was attenuated by 56% and 42%, respectively. Two minutes after unclipping and bleeding when necessary, mean arterial pressure decreased from 171 +/- 11 to 134 +/- 11 mm Hg and remained at approximately the same level for the 2-hour period of observation. The extent of reversal of the mean pressure threshold for activation of the baroreceptors was approximately constant (approximately 60%) in the time range of 2-120 minutes. The extent of reversal was slightly higher when the changes in systolic pressure threshold divided by the total change in control diastolic pressure were calculated (maximal of 83%). During the first 20 minutes, the displacements of the curves were parallel with no change in the depressed gain sensitivity. Complete normalization of gain sensitivity was observed after 90-120 minutes. The data indicate that, within the first 2 hours of pressure normalization of chronic renal hypertensive rats, 1) reversal of the resetting of pressure threshold is pronounced (60-80%) but still incomplete and 2) gain sensitivity returns completely to normal.

Animals↗
PubMed1989

Extent of rapid baroreceptor resetting during first hours of hypertension.

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.

Animals↗
PubMed1988

Characteristics and extent of rapid aortic baroreceptor resetting in rat.

The characteristics of rapid or acute resetting of the aortic baroreceptors were studied in anesthetized rats during 30 minutes of sustained hypertension produced by phenylephrine infusion. Two minutes after the onset of hypertension, a resetting of 26% (ratio of change in systolic threshold pressure to total change in diastolic pressure) was demonstrable. This represents 60% of the maximal resetting (43%) observed after 20 minutes. Thereafter, the magnitude of resetting remained stable. Pressure-nerve activity showed a parallel shift after 2 and 20 minutes of hypertension, with a slight tendency to increased slope at elevated pressures, especially in the baroreceptor function curve analyzed after 2 minutes. These results suggest that in rats, no significant difference exists in the time course for resetting of baroreceptor fibers with low vs. high thresholds. In contrast to other studies, reversibility of the resetting process was not complete within 30 minutes of pressure normalization, and the extent of reversal was no greater than 60%. The data of the present study, taken together with those obtained previously after 6 hours of hypertension, suggest that during the onset and maintenance of hypertension in rat, acute or rapid resetting of the baroreceptors reaches its maximum in 20 minutes (40%) and remains stable for up to 6 hours, with no apparent change in the baroreceptor gain.

Animals↗