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Heart rate effect of angiotensin II involves the area postrema and central alpha-1 adrenergic mechanisms
WS6-B2-1-04 HEART RATE EFFECT OF ANGIOTENSIN MECHANISMS
II INVOLVES THE AREA POSTREMA AND CENTRAL ALPHA-I ADRENERGIC
M. Ryuzaki I, V.S. Bishop I, H. Suzuki 2, T. Saruta 2 i) Dept. of Physiology, Univ. of Texas Health Science Center, San Antonio, of Internal Medicine, School of Medicine, Keio Univ., Tokyo, Japan
Texas, U.S.A.
2) Dept.
Several studies show that angiotensin II (Ang II) resets the operating point of the heart rate (HR)-baroreflex function to higher arterial pressures. This resetting depends upon the area postrema (AP) and can be blocked by the alpha-i antagonist, prazosin. The purpose of this study was to determine the mechanism of this resetting. The studies were performed in intact, sinoaortic denervated (SAD), AP-lesioned (APX) and SAD + APX rabbits. All rabbits were chronically instrumented with an arterial catheter in the abdominal aorta and a venous catheter in the inferior vena cava. SAD performed at least 1 week prior to catheterization and APX was performed at least 3 weeks before catheterization. Experiments were performed 1 week following catheterization. Ang II (2.5 - i00 ng/kg/min) was infused intravenously or intravertebrally to conscious intact, APX, SAD and SAD + APX rabbits before and after intravertebral prazosin (i0 Bg/kg). In intact rabbits, Ang II produced dose dependent increases in blood pressure. HR was little affected except at the highest dose (i00 ng/kg/min). In APX rabbits, intravertebral Ang II (i00 ng/kg/min) produced large decreases in HR (from 246+8 bpm to 179~12 bpm, P
WS6-B2-1-05 ACUTE MODIFICATION OF BAROREFLEX CONTROL OF RENAL SYMPATHETIC NERVE ACTIVITY DURING WATER IMMERSION IN CONSCIOUS DOGS. K. Miki I , Y. Hayashida 2 and K. Shiraki 2 I) Dept. of Environs. Health, Life Science and Human Technology, Nara Women's Univ. Nara 630, Japan 2)Dept. of Physiol. Univ. Occup. and Environ. Health, Kitakyushu 807, Japan. The purpose of the present study was to evaluate an acute modification of baroreflex control of renal sympathetic nerve activity (RSNA) during WI in conscious dogs. The dogs (n=9) were instrumented chronically with a stainless steel electrode for the measurements of RSNA and carotid sinus nerve activity (CSNA) and three catheters for the m e a s u r ~ e n t s of systemic arterial pressure at renal level (Pa), mean carotid arterial pressure (Pmca) and central venous pressure (Pcv). The experiment consisted of a 60-min control period in air, 120 min of WI, and a 60-in recovery period in air. The dogs were immersed to the midcervical level under thermoneutral condition. The relationships of both Pmca-RSNA and Pmca-CSNA were studied by raising and lowering systemic arterial pressure by administrations of phenylephrine (150 mg iv.) and nitroprusside (300 mg iv.), respectively, before the control period, 90 min of WI and after the recovery period. Relationship between Pmca and RSNA was quantified by fitting obtained values to a si~noidal equation; Pmca=A1/(I+exp(A2(X-A3))+A4; where X is RSNA; A1, a range of Pmca; A2, a gain of Pmca-RSNA response; A3, a midpoint pressure (Pmca at the maximum gain); A4, a minimum value of Pmca. The relationship of Pmca-CSNA was analyzed similarly to study a nature of transduction process in carotid sinus baroreceptors during WI. WI induced an acute modification of carotid sinus baroreflex control of RSNA, because the gain increased by 84%, the midpoint pressure decreased by 17 ~ g , whereas the range and the minimum value of Pmca were constant. The Pmca-CSNA curve did not change throughout the experimental period. This indicates that the nature of transduction of arterial pressure in carotid sinus baroreceptors did not change during WI. Therefore, it is likely that WI induces an acute modification of baroreflex control of RSNA at site of the supra-carotid baroreceptors. WI increased Pcv by 10.0 ± 0.1 nm~g in a step manner in the present experiment. This suggests cardiopulmonary baroreceptors are loaded which in turn increased their afferent signal to the central nervous system throughout the WI. The loading of left atrial mechanoreceptors by balloon inflation decreased RSNA in sustained manner (Miki et al, Am. J. Physiol. 264:R369-R375, 1993). Furthermore, we have shown previously that WI decreased RSNA by 43% throughout the period of WI (Miki et al. Am. J. Physiol. 256:R299-R305, 1989). It is therefore concluded the acute modification of baroreflex control of RSNA might be caused by an interaction within central nervous system with afferent input originating from cardiopulmonary mechanoreceptors without carotid sinus baroreceptors themselves to be reset.
376
II INVOLVES THE AREA POSTREMA AND CENTRAL ALPHA-I ADRENERGIC
M. Ryuzaki I, V.S. Bishop I, H. Suzuki 2, T. Saruta 2 i) Dept. of Physiology, Univ. of Texas Health Science Center, San Antonio, of Internal Medicine, School of Medicine, Keio Univ., Tokyo, Japan
Texas, U.S.A.
2) Dept.
Several studies show that angiotensin II (Ang II) resets the operating point of the heart rate (HR)-baroreflex function to higher arterial pressures. This resetting depends upon the area postrema (AP) and can be blocked by the alpha-i antagonist, prazosin. The purpose of this study was to determine the mechanism of this resetting. The studies were performed in intact, sinoaortic denervated (SAD), AP-lesioned (APX) and SAD + APX rabbits. All rabbits were chronically instrumented with an arterial catheter in the abdominal aorta and a venous catheter in the inferior vena cava. SAD performed at least 1 week prior to catheterization and APX was performed at least 3 weeks before catheterization. Experiments were performed 1 week following catheterization. Ang II (2.5 - i00 ng/kg/min) was infused intravenously or intravertebrally to conscious intact, APX, SAD and SAD + APX rabbits before and after intravertebral prazosin (i0 Bg/kg). In intact rabbits, Ang II produced dose dependent increases in blood pressure. HR was little affected except at the highest dose (i00 ng/kg/min). In APX rabbits, intravertebral Ang II (i00 ng/kg/min) produced large decreases in HR (from 246+8 bpm to 179~12 bpm, P
WS6-B2-1-05 ACUTE MODIFICATION OF BAROREFLEX CONTROL OF RENAL SYMPATHETIC NERVE ACTIVITY DURING WATER IMMERSION IN CONSCIOUS DOGS. K. Miki I , Y. Hayashida 2 and K. Shiraki 2 I) Dept. of Environs. Health, Life Science and Human Technology, Nara Women's Univ. Nara 630, Japan 2)Dept. of Physiol. Univ. Occup. and Environ. Health, Kitakyushu 807, Japan. The purpose of the present study was to evaluate an acute modification of baroreflex control of renal sympathetic nerve activity (RSNA) during WI in conscious dogs. The dogs (n=9) were instrumented chronically with a stainless steel electrode for the measurements of RSNA and carotid sinus nerve activity (CSNA) and three catheters for the m e a s u r ~ e n t s of systemic arterial pressure at renal level (Pa), mean carotid arterial pressure (Pmca) and central venous pressure (Pcv). The experiment consisted of a 60-min control period in air, 120 min of WI, and a 60-in recovery period in air. The dogs were immersed to the midcervical level under thermoneutral condition. The relationships of both Pmca-RSNA and Pmca-CSNA were studied by raising and lowering systemic arterial pressure by administrations of phenylephrine (150 mg iv.) and nitroprusside (300 mg iv.), respectively, before the control period, 90 min of WI and after the recovery period. Relationship between Pmca and RSNA was quantified by fitting obtained values to a si~noidal equation; Pmca=A1/(I+exp(A2(X-A3))+A4; where X is RSNA; A1, a range of Pmca; A2, a gain of Pmca-RSNA response; A3, a midpoint pressure (Pmca at the maximum gain); A4, a minimum value of Pmca. The relationship of Pmca-CSNA was analyzed similarly to study a nature of transduction process in carotid sinus baroreceptors during WI. WI induced an acute modification of carotid sinus baroreflex control of RSNA, because the gain increased by 84%, the midpoint pressure decreased by 17 ~ g , whereas the range and the minimum value of Pmca were constant. The Pmca-CSNA curve did not change throughout the experimental period. This indicates that the nature of transduction of arterial pressure in carotid sinus baroreceptors did not change during WI. Therefore, it is likely that WI induces an acute modification of baroreflex control of RSNA at site of the supra-carotid baroreceptors. WI increased Pcv by 10.0 ± 0.1 nm~g in a step manner in the present experiment. This suggests cardiopulmonary baroreceptors are loaded which in turn increased their afferent signal to the central nervous system throughout the WI. The loading of left atrial mechanoreceptors by balloon inflation decreased RSNA in sustained manner (Miki et al, Am. J. Physiol. 264:R369-R375, 1993). Furthermore, we have shown previously that WI decreased RSNA by 43% throughout the period of WI (Miki et al. Am. J. Physiol. 256:R299-R305, 1989). It is therefore concluded the acute modification of baroreflex control of RSNA might be caused by an interaction within central nervous system with afferent input originating from cardiopulmonary mechanoreceptors without carotid sinus baroreceptors themselves to be reset.
376