scholarly journals Impaired cardiopulmonary baroreflex control of renal nerves in renal hypertension.

1985 ◽  
Vol 57 (5) ◽  
pp. 741-747 ◽  
Author(s):  
M D Thames ◽  
L N Johnson
1994 ◽  
Vol 266 (1) ◽  
pp. R27-R39 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin

Efferent renal sympathetic nerve activity (ERSNA) is increased in the rat with low-cardiac-output congestive heart failure (CHF; myocardial infarction). Arterial and cardiopulmonary baroreflex control of ERSNA in CHF and control rats was examined. Cardiac index and arterial pressure were lower and total peripheral resistance index, left ventricular end-diastolic pressure, and heart-to-body weight ratio were higher in CHF than in control rats. Increases in left ventricular end diastolic pressure produced by intravenous volume loading failed to increase cardiac index in CHF rats as it did in control rats. Single-unit analysis of aortic baroreceptor nerve activity showed that CHF rats had higher pressure threshold, lower frequency at pressure threshold, and lower gain than control rats. Arterial baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. Single-unit analysis of vagal nerve activity showed that CHF rats had higher pressure threshold, lower frequency at saturation, and lower gain than control rats. Cardiopulmonary baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. In the CHF rat, arterial and cardiopulmonary baroreflex control of ERSNA is markedly attenuated because of abnormalities in the periphery at the level of the aortic and cardiopulmonary receptors, respectively, and not in the central nervous system.


1983 ◽  
Vol 245 (3) ◽  
pp. H420-H428 ◽  
Author(s):  
G. B. Guo ◽  
M. D. Thames

We determined if baroreflex control (BC) of lumbar sympathetic nerve activity (LSNA) is preserved despite impaired control of heart rate (HR) in rabbits with 6 wk of renal hypertension (HT). Baroreflex responses were determined during transient or steady-state increases (phenylephrine, PE) or decreases (nitroglycerin or caval occlusion) in arterial pressure. Impaired BC of HR was confirmed in conscious and anesthetized HT rabbits with all baroreflexes intact. In contrast, BC of LSNA was preserved in anesthetized HT rabbits. We further determined whether this selective impairment of BC of HR but not of LSNA could be due to an abnormality in the central nervous system (CNS) or in the afferent limb of the baroreflex. With only the left aortic depressor nerve (ADN) intact (other arterial baroreceptor afferents cut), BC of both HR and LSNA in HT was significantly impaired during infusion of PE. However, responses of HR and LSNA to afferent electrical stimulation of the left ADN (all arterial baroreceptor afferents cut) were similar in HT and normotensive controls. We conclude that 1) BC of LSNA is preserved in renal HT even though control of HR is impaired; 2) selective impairment of BC of HR in HT results from an abnormality in the afferent limb of baroreflex and not in CNS; 3) this abnormality in the afferent limb is not sufficient to impair BC of LSNA when all baroreflexes are intact but is sufficient after partial arterial baroreceptor denervation.


1997 ◽  
Vol 273 (2) ◽  
pp. R457-R471 ◽  
Author(s):  
J. L. Segar

The autonomic nervous system is intimately involved in regulating cardiovascular function. Sensing mechanisms dispersed throughout the circulation, including arterial baroreceptors, low pressure receptors, and chemosensitive receptors, continually evoke reflexes designed to maintain cardiovascular homeostasis. Although there is a growing body of knowledge regarding neural regulation of the adult cardiovascular system, characterization and understanding of these physiological systems during development is limited. This review highlights developmental changes in the arterial and cardiopulmonary baroreflex during fetal and postnatal life and contrasts the function of these responses with those seen in the adult. Baroreceptors are functional in the immature animal and reset toward higher pressure levels with maturation. In our ovine model, the sensitivity of the efferent limb of the baroreflex is greatest during fetal life and decreases with postnatal development. As in the adult, angiotensin II and arginine vasopressin interact with the sympathetic nervous system early during development to alter baroreflex control of the cardiovascular system. However, the extent to which these hormonal systems influence autonomic reflexes during the fetal and newborn period appears vastly different than in the adult. Endogenous angiotensin II significantly contributes to resetting of the arterial baroreflex early in life, whereas even high circulating levels of vasopressin have little effect on baroreflex function until adulthood. Finally, the ability of cardiopulmonary mechanoreceptors to regulate cardiovascular function is impaired early in development, in sharp contrast to the heightened sensitivity of the arterial baroreflex at this stage of maturation. The potential importance of these autonomic reflexes on cardiovascular function during the perinatal period is highlighted.


1981 ◽  
Vol 241 (3) ◽  
pp. H332-H336
Author(s):  
M. D. Thames ◽  
C. L. Eastham ◽  
M. L. Marcus

The purpose of this study is to determine if baroreflex control of heart interval is abnormal in conscious dogs with renal hypertension. Changes in heart interval in response to transient nitroglycerin-induced decreases in arterial pressure and transient phenylephrine-induced increases in arterial pressure were determined in nine normotensive [mean arterial pressure 92 +/- 4 (SE) mmHg] and nine renal hypertensive conscious dogs (mean arterial pressure 139 +/- 10 mmHg). Data were acquired before and after beta-adrenergic blockade with 2 mg/kg iv propranolol and before and after parasympathetic blockade with 0.5 mg/kg iv atropine. Control heart rates for the normotensive and hypertensive dogs were not different (91 +/- 4 and 93 +/- 7 beats/min, respectively). Before autonomic blockade, the responses of normotensive and hypertensive dogs to nitroglycerin were not different. However, prolongation of the heart interval in response to phenylephrine in hypertensive dogs was significantly less than in normotensive dogs. In both groups, atropine nearly abolished the decrease in heart interval in response to nitroglycerin and the increase in heart interval in response to phenylephrine, although there were small but significant residual responses. Propranolol was without significant effect on heart interval responses to nitroglycerin and phenylephrine. We conclude that the baroreflex control of heart interval during transient decreases in arterial pressure is preserved in hypertensive dogs and is mediated mainly by decreases in parasympathetic outflow to the heart. In contrast, baroreflex control of heart interval during transient increases in arterial pressure is impaired in hypertension and is mediated mainly by activation of parasympathetic cholinergic mechanisms.


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