Effect of age on myocardial adaptation to volume overload in the rat.

Isoyama, Shogen; Grossman, William; Wei, Jeanne Y.

doi:10.1172/jci113530

Cited by 88 publications

(40 citation statements)

References 35 publications

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“…We did not measure LVEDP continuously during the experiments to assess the sensitivity of cardiopulmonary reflexes because left ventricular catheterization may harm the aortic valve, thus altering the hemodynamics of the left ventricle. 20 For all other experiments the rats were equipped as described above (one arterial and two femoral venous catheters, renal nerve electrode). The arterial catheter was connected to a Statham P23 Db transducer for continuous recording of blood pressure and heart rate (HR).…”

Section: Protocolmentioning

confidence: 99%

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

et al. 1994

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We hypothesized that impaired cardiopulmonary reflexes but not altered baroreceptor reflexes precede deoxycorticosterone acetate (DOCA)-salt hypertension. Uninephrectomized rats were given either DOCA and 0.9% NaCl as drinking water, 0.9% NaCl alone, or tap water. We measured mean blood pressure, heart rate, and renal sympathetic nerve activity. After 8 days, mean blood pressure was not different in DOCA-salt and control rats. Volumesensitive cardiopulmonary reflexes were tested by intravenous volume loading with saline (10% body weight in 15 minutes), which decreased renal sympathetic nerve activity without changing mean blood pressure or heart rate. This response was blunted in DOCA-salt rats. Chemosensitive cardiopulmonary reflexes were tested by 15-minute infusions of the serotonin 5-HT 3 agonist phenylbiguanide, which decreased renal sympathetic nerve activity without changing mean blood pressure or heart rate. Sustained decreases in A ltered central sympathetic outflow and decreased reflex control of peripheral sympathetic nerves are thought to be associated with established hypertension 14 ; however, the distinction between cause and effect is unclear. 5- 6 The sympathetic nervous system could influence blood pressure control not only by its effect on the regulation of peripheral resistance but also by controlling volume homeostasis via efferent renal sympathetic nerve activity (RSNA). -8It is well established that RSNA influences tubular water and sodium reabsorption independent of changes in intrarenal and systemic hemodynamics.2 -9 An increase in RSNA augments sodium and water reabsorption, consequently decreasing urinary flow and salt excretion. A decrease in RSNA leads to opposite effects. Thus, an impairment of RSNA regulation could alter volume homeostasis and thereby contribute to the development of hypertension. 10The activity of renal sympathetic nerve fibers is specifically controlled by cardiopulmonary reflexes. In the rat, prolonged stimulation of volume-sensitive cardiopulmonary reflexes with isotonic volume expansion inhibits RSNA but not the efferent activity of sympathetic fibers controlling peripheral resistance. -11The aim of the present study was to elucidate the putative role of these cardiopulmonary reflexes in the Received November 2, 1993; accepted in revised form June 29, 1994.From the Department of Internal Medicine, University of Erlangen-Niirnberg (Germany).Correspondence to Roland Veelken, MD, Nephrology Laboratory, Department of Medicine IV, University of Erlangen-Niirnberg, LoschgestraBe 8Vi, 91054 Erlangen, FRG.© 1994 American Heart Association, Inc.renal sympathetic nerve activity occurred during phenylbiguanide infusion in controls but were blunted over time in DOCA-salt rats. The arterial baroreflex responses to graded infusions of methoxamine and nitroprusside were analyzed by sigmoidal curve fitting. There were no differences in gain of renal sympathetic nerve activity or heart rate between the groups. Thus, DOCA-salt rats exhibit impaired cardiopulmonary ref...

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Section: Protocolmentioning

confidence: 99%

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

et al. 1994

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“…Each rat was anesthetized with pentobarbital sodium (50 mg/kg i.p.) and endotracheal intubation was performed with direct visualization as in the previous study (35,36). The left thorax was opened at the third intercostal space to expose the ascending aorta under artificial ventilation with room air (model 141; Princeton Medical Instruments Inc., Natick, MA).…”

Section: Methodsmentioning

confidence: 99%

“…A polyethylene cannula (polyethylene tubing, SP-3 1, 0.50 mm i.d., 0.80 mm o.d. ; Natsume Instrument Co., Ltd., Tokyo, Japan) was inserted into the right carotid artery to measure aortic pressure as in the previous study (35,36). To estimate left ventricular peak systolic and end-diastolic pressures, and the peak-to-peak pressure difference between the left ventricle and the aorta, a left thoracotomy was performed at the fourth intercostal space.…”

Section: Methodsmentioning

confidence: 99%

Complete reversibility of physiological coronary vascular abnormalities in hypertrophied hearts produced by pressure overload in the rat.

Isoyama

Ito²,

Kuroha³

et al. 1989

J. Clin. Invest.

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“…Functionally, decreased coronary flow/unit myocardial mass, 4 -5 decreased flow reserve in response to reactive hyperemia, adenosine, or sodium nitroprusside administration, 6 -8 increased coronary vascular resistance/unit muscle mass, and lower perfusion in the endocardium 9 occur. At the same time, aging causes myocardial hypertrophy at organ 410 - 11 and cellular levels 4 -10 - 12 and cell loss. 12 Functionally, agerelated decreases in the rate of tension rise and increases in duration of contraction force or de-creases in shortening velocity have been reported at organ and muscle levels.…”

Section: Effect Of Age On Coronary Circulation After Imposition Of Prmentioning

confidence: 99%

Effect of age on coronary circulation after imposition of pressure-overload in rats.

1991

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We examined the effects of pressure overload on coronary circulation in young adult (7 months old) and old rats (18 months old). Four weeks after the ascending aorta was banded, in vivo left ventricular pressure was measured to estimate the degree of pressure load. In the two age groups, similar increases in peak left ventricular pressure were observed (113 ±7 mm Hg in sham-operated rats versus 160 ±11 mm Hg in banded rats of the young adult group; 103 ±7 mm Hg in sham-operated rats versus 156±11 mm Hg in banded rats of the old group). After isolating the hearts, they were perfused with Tyrode's solution containing bovine red blood cells and albumin. Resting coronary perfusion pressure-flow relations and reactive hyperemic response after a 40-second ischemia were obtained under beating but nonworking conditions. In young adult banded rats, significant myocardial hypertrophy was observed at the organ level (124% of controls in left ventricular dry weight/body weight ratio; 119% in left ventricular dry weight/tibial length ratio) and at the cell level. Minimal coronary vascular resistance obtained by the perfusion pressure-peak flow relation during reactive hyperemia increased to 150% of controls, and coronary flow reserve decreased significantly. In contrast, myocardial hypertrophy was not observed at the organ or cell level in old banded rats. However, minimal coronary vascular resistance increased, and flow reserve decreased significantly. Thus, pressure overload with coronary arterial hypertension caused abnormalities of the coronary circulation in old subjects even in the absence of myocardial hypertrophy. These coronary vascular changes as well as diminished hypertrophic response may explain the high incidence of heart failure or ischemic episodes during chronic hemodynamic stress in aged patients. Address for reprints: Tamotsu Takishima, MD, First Department of Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai 980, Japan.Received February 19, 1990; accepted in revised form November 6, 1990. creases in shortening velocity have been reported at organ and muscle levels.413 -17 Furthermore, the capacity for myocardial hypertrophy to develop in response to chronic pressure-or volume-overload is diminished in aged subjects compared with younger adults. 10-11 -18 -19 At present, however, there is no information concerning the coronary vascular response to stress from chronic pressure overload in aged subjects.Abnormalities of the coronary circulation in pressure-overloaded hearts are caused by hypertensive vascular changes 20 -21 as well as by the presence of myocardial hypertrophy. 22-24 Therefore, even if a similar pressure-overload stress is applied to young adult and old subjects, the stress may produce different effects on coronary circulation between young and old subjects directly through underlying agerelated changes in coronary vasculature or indirectly through the diminished myocardial hypertrophic response. To test this hypothesis, we examined the effects of pr...

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Effect of age on myocardial adaptation to volume overload in the rat.

Cited by 88 publications

References 35 publications

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

Impaired cardiovascular reflexes precede deoxycorticosterone acetate-salt hypertension.

Complete reversibility of physiological coronary vascular abnormalities in hypertrophied hearts produced by pressure overload in the rat.

Effect of age on coronary circulation after imposition of pressure-overload in rats.

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