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Biomedical subjects

E M Krieger

Publications and source records attributed to E M Krieger.

At least 19 recordsLinked to original sources
PubMed1992

Carotid chemoreceptors influence arterial pressure in intact and aortic-denervated rats.

The objective of the present study was to analyze the role of the arterial chemoreceptors in arterial pressure alterations produced by sinoaortic denervation (SAD) in rats. The mean arterial pressure during 2 h of continuous computerized beat-to-beat recordings was higher after aortic denervation (AD; 130 +/- 2 and 124 +/- 3 mmHg, respectively), lower after sinus denervation (SD; 101 +/- 1 and 101 +/- 3 mmHg), and remained unaltered after SAD (121 +/- 3 and 108 +/- 2 mmHg) 1 and 20 days after denervation compared with control rats (114 +/- 1 mmHg). Hypotensive effect of SD was confirmed when arterial pressure was recorded in the same animal before and after SD (from 112 +/- 2 to 103 +/- 2 mmHg). A similar effect was observed after isolated carotid body artery (CBA) ligation (from 114 +/- 3 to 104 +/- 3 mmHg). Furthermore, CBA ligation attenuated by 13% the hypertension after AD (from 136 +/- 2 to 118 +/- 3 mmHg). Bradycardic response to phenylephrine and arterial pressure variability were markedly altered by SAD and AD but remained normal after SD. In contrast, the chemoreflex (intravenous KCN) was abolished after SAD, SD, and CBA ligation but was preserved after AD. These data suggest that the arterial pressure alteration produced by SAD in rats represents the net effect of the abolition of inhibitory (baroreceptor deafferentation) and excitatory (chemoreceptor deafferentation) influences on the arterial pressure.

Animals↗
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

Angiotensin converting activity assessed in vivo is increased in hereditary hypertensive rats.

1. The angiotensin converting enzyme (ACE) activity of spontaneously hypertensive (SHR) and spontaneously hypertensive stroke-prone (SHRSP) rats was compared to the ACE activity of normotensive Wistar-Kyoto rats (WKY). 2. ACE activity was assessed indirectly in conscious unrestrained rats using the equipressor response end point to simultaneously calculate the extent of conversion of angiotensin I (AI) to angiotensin II (AII) and the pulmonary degradation of bradykinin (BK). 3. The pulmonary degradation of BK was significantly elevated (99.4%) in SHR rats whereas the elevation was not significant in SHRSP rats (99.2%) compared to WKY rats, even though the pulmonary inactivation of BK in WKY rats was higher (98.6%) than in normotensive Wistar rats (95.6% and 97.5%) previously studied. 4. Blood pressure responsiveness to intra-aortically injected BK (bolus injection and infusion) was markedly increased in SHR and SHRSP rats with no change in reactivity to sodium nitroprusside. 5. Conversion of AI to AII assessed by the equipressor doses of the hormones which produced a 20-mmHg rise in blood pressure was markedly elevated in SHR (86 +/- 4%) and SHRSP (80 +/- 7%) rats when compared to WKY rats (38 +/- 4%). 6. The marked increase in conversion of AI to AII in hypertensive animals, accompanied by an increased pulmonary degradation of BK in SHR rats, suggests that ACE activity is increased in conscious SHR and SHRSP rats and may participate in the genesis of hypertension in this model of genetic hypertension.

Angiotensin I↗
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

Reversal of hyperreactivity to bradykinin in renal hypertensive rats.

Increased blood pressure responsiveness to bradykinin in comparison with other vasodilator agents was demonstrated in rats with long-term one-kidney and two-kidney, one clip hypertension. In the present study, we analyzed the reactivity to intra-aortically injected bradykinin in unanesthetized one-kidney, one clip hypertensive rats during the control period and 1, 5, and 8 hours after reversal of hypertension after removal of the renal artery constriction. One and 5 hours after unclipping the renal artery, the mean blood pressure decreased markedly (from 195 +/- 7 to 124 +/- 8 and 145 +/- 9 mm Hg, respectively), whereas the hyperreactivity to bradykinin reverted only slightly, and the responses to nitroprusside remained unchanged. In another group of hypertensive rats examined 8 hours after unclipping (pressure decreased from 192 +/- 4 to 143 +/- 8 mm Hg), the hyperreactivity to bradykinin had partially reverted. Significantly larger doses of bradykinin were necessary to produce the same decrease in blood pressure when compared with the control period (16.4 +/- 2.0 vs. 7.2 +/- 1.2 ng). The same degree of reversal of hyperreactivity to bradykinin was observed when the blood pressure of hypertensive rats was reduced (from 207 +/- 8 to 143 +/- 5 mm Hg) during 1 hour by hydralazine injection. Complete reversibility of bradykinin hyperreactivity was produced by nitroprusside infusion (from 201 +/- 13 to 142 +/- 10 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

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↗
PubMed1990

Influence of general anesthetics on baroreflex control of circulation.

1. The effects of sodium pentobarbital and alpha-chloralose anesthesia on the baroreflex control of circulation were studied in groups of 7 to 11 rats. The tests were performed in conscious undisturbed rats and repeated after anesthesia. 2. Pentobarbital (15 min) depressed the initial peak of the pressor response produced by carotid occlusion by 68% (15 +/- 1 vs 47 +/- 3 mmHg) and the maintained response by 52% (13 +/- 1 vs 27 +/- 4). Depression by chloralose was 48% (26 +/- 5 vs 50 +/- 3) and 21% (19 +/- 2 vs 24 +/- 3), respectively. The inhibition progressively declined at 30, 60, 90 and 120 min after pentobarbital but was unchanged up to 120 min after chloralose. 3. The baroreflex sensitivity index for bradycardic responses (phenylephrine injection) diminished by 50% after pentobarbital (-1.1 +/- 0.3 vs -2.2 +/- 0.3 beats/min per mmHg) and remained unaltered after chloralose. 4. The baroreflex sensitivity index for tachycardic responses (nitroprusside injection) was depressed by 61% after pentobarbital (-1.5 +/- 0.5 vs -3.8 +/- 0.5 beats/min per mmHg) and 35% after chloralose (-2.5 +/- 0.2 vs -3.9 +/- 0.5). 5. In general the depression of reflex control of circulation was more severe after pentobarbital than after chloralose anesthesia, while the resting control arterial pressure was not affected by either. The inhibition of the baroreflex tachycardic responses was more intense than that of the bradycardic responses and represented a better index of the depression exerted on the pressure responses to carotid occlusion.

Animals↗
PubMed1989

Arterial baroreceptor resetting in hypertension (the J. W. McCubbin memorial lecture).

1. The arterial baroreceptors are reset to operate at higher pressure levels in hypertension. Rapid (acute) resetting occurs within the first few minutes after elevation of arterial pressure, but is only partial because the increased threshold for baroreceptor activation represents only 25-50% of the arterial pressure increase. 2. Complete resetting occurs when the increase in pressure threshold equals the increase in arterial pressure; in the rat this is present after 48 h hypertension. 3. The aortic calibre was studied in freely moving rats; the time taken for the diastolic calibre to reach maximum dilation correlated with the time taken for complete resetting of the threshold of the aortic baroreceptors. During transient pressure increases the displacement of the diastolic calibre was much greater than the increase in pulsation, indicating that, under physiological conditions, sustained distension of the diastolic calibre is an important factor in aortic baroreceptor distortion. 4. The relative change of the diastolic calibre, in relation to control calibre, remains relatively constant during transient pressure changes in aortae of increased calibre produced by chronic hypertension or growth. 5. It is concluded that complete resetting of the baroreceptors in hypertension occurs when the increased stress on the arterial wall is matched by a proportional increase in diastolic calibre.

Animals↗
PubMed1989

Changes in plasma ACE activity during the development and reversal of one-kidney, one clip hypertension in rats.

Plasma angiotensin converting enzyme (ACE) activity was studied during the development and the reversal of one-kidney, one clip (1K1C) renal hypertension in rats (RHR). Plasma ACE activity was measured in RHR 1 (n = 11), 3 (n = 8), 6 (n = 12), 14 (n = 7), and 80-120 days (n = 17) after clipping. Plasma ACE activity (nmol/min/ml) was elevated (p less than 0.05) in chronic RHR (80-120 days; mean arterial pressure, MAP: 216 +/- 9 mmHg), being 142 +/- 14 (n = 17) vs. 100 +/- 3.2 (n = 20) for normotensive control rats (MAP: 116 +/- 3 mmHg), whereas no significant differences were observed at earlier times. Overactivity of the renin-angiotensin system (RAS) was demonstrated indirectly by the reduction of MAP (greater than 15 mmHg) in response to captopril (10 mg/kg, i.v.) only during the first 3 days after clipping and in chronic severely hypertensive rats. In another experiment, ACE activity in chronic RHR was measured serially before and 1, 6 and 24 hours after unclipping. Serial measurements of plasma ACE showed a progressive decrease from 145 +/- 26 to 122 +/- 21, 24 hours after unclipping (n = 7, p less than 0.05, paired Student t-test) when MAP was reduced from 204 +/- 15 to 113 +/- 7 mmHg. There was essentially no change during 24 hours from the initial values of RHR-sham (MAP: 206 +/- 5 mmHg, ACE: 140 +/- 19, n = 8) and normal rats-sham (MAP: 115 +/- 2 mmHg, ACE: 96 +/- 3, n = 6). These data provide further evidence that chronic renal hypertension is associated with important changes in the metabolism of vasoactive peptides.

Animals↗
PubMed1987

Alteration in baroreceptor function in rats produces typical pressure changes during sleep.

We have shown previously that both sinoaortic denervation (SAD) and high renin hypertension in the rat produce a pronounced alteration in the pattern of pressure change during sleep, namely from unchanged to a rise in pressure during synchronized sleep (SS) and from a slight rise to a marked fall during desynchronized sleep (DS). Since acute SAD also produces overactivity of the renin-angiotensin system (RAS), we investigated if this overactivity is essential for the development of the alterations. In rats studied 1 day after SAD (138 +/- 1.0 mm Hg) the MAP rose during SS (+14 +/- 0.7 vs. +1.0 +/- 0.16 mm Hg in the controls) and fell during DS (-27.2 +/- 1.5 vs. 4.9 +/- 0.6 mm Hg in the controls). Captopril-treated rats, studied 1 day after SAD (89 +/- 1.2 mm Hg), also exhibited rise in pressure during SS (+12.3 +/- 0.6 mm Hg) and fall during DS (-12.8 +/- 1.7 mm Hg). Similar alterations were observed in rats studied 10 days after SAD (116 +/- 0.7 mm Hg) when RAS activity was normal (PRA: 1.3 +/- 0.2 vs. 10.4 +/- 2.7 ng AI/ml/h for SAD-1 day); the MAP rose during SS (+6.5 +/- 0.3 mm Hg) and fell during DS (-5.0 +/- 0.9 mm Hg). These data indicate that impairment of the baroreceptor function per se determines the typical alteration in the pattern of pressure change during sleep in the rat.

Animals↗
PubMed1977

Role of the baroreceptor reflex in the early phases after removing the renal artery constriction in conscious renal hypertensive rats.

Hemodynamic studies in unanesthetized rats with chronic one-kidney-Goldblatt hypertension showed a 25% increase in cardiac output and a 42% increase in peripheral resistance. Removal of renal artery constriction under either anesthesia and minor surgical trauma produced an immediate 20% drop in arterial pressure. At the end of the 6 observation period the pressure dropped 30% but still remained at a moderate hypertensive level. The hemodynamic measurement at that time suggested that the pressure drop was the result of a decrease in cardiac output. However, the data obtained 1 hour after removal of the constriction suggested that a vasodilating mechanism may also contribute to pressure normalization in the early phase of reversal of renal hypertension. In the sham-operated hypertensive rats the pressure remained unchanged, while the cardiac output dropped due to compensation by a proportional increase in peripheral resistance. In contrast, in the unclipped animals the same drop in cardiac output produced an equivalent fall in pressure because no change in peripheral resistance occurred. This was not due to an insufficiency of the baroreceptor reflex since bilateral splanchnicectomy performed at that time produced a striking hypotensive response, indicating an overactivity of the sympathetic system possibly due to the baroreceptor still reset to operate at a hypertensive level.

Animals↗
PubMed1977

Continuous measurement of aortic caliber in conscious rats. Effect of acute hypertension.

For continuously measuring the circumference of the aorta in conscious rats for up to 20 days, a new electrolytic strain gauge of high sensitivity and stability was constructed of silicone tubing filled with copper nitrate. The mean systolic and diastolic circumferences measured in 11 nonanesthetized undisturbed rats were 6.557 +/- 0.128 mm and 6.533 +/- 0.128 mm, respectively--the pulse pressure (51 mm Hg) producing an increase of 0.024 mm in aortic size (0.37% increase of the diastolic circumference). The calculated dynamic elastic modulus was 13,908 dynes/cm2. Infusions of blood, angiotensin, and noradrenaline to increase mean aortic pressure acutely by 50 mm Hg caused aortic circumference to increase by 0.59, 0.58, and 0.53%, respectively. Seven rats were subjected to acute hypertension produced by subdiaphragmatic aortic constriction after recording the control measurements. Over the period of study (6 hours) after aortic constriction, mean aortic blood pressure was increased 50 mm Hg from the control of 101 mm Hg. A mean maximal increase of 6% in aortic circumference was seen at 3 hours and a mean minimum of 0.9% at 4 hours, with an average increase of 3% for the entire 6-hour period. These changes in aortic circumference coincide with an upward displacement of about 30% in the range of activation of the aortic baroreceptors.

Animals↗
PubMed1976

Resetting of the baroreceptor in hypotension in rats.

1. A progressive but incomplete adaptation of the aortic baroreceptor was observed after 1 and 6 h of hypotension in rats subjected to controlled bleeding. Administration of phenoxybenzamine produced a greater downward displacement of baroreceptor activation range. 2. Complete adaptation was observed after 48 h of maintained hypotension in rats treated with reserpine. 3. The range of the aortic baroreceptor activation shifted upward as pressure returned to normotension, indicating the reversibility of baroreceptor adaptation in hypotension.

Adaptation, Physiological↗