Sympathetic changes during development of cardiac hypertrophy in aortic-constricted rats

1988 ◽  
Vol 255 (3) ◽  
pp. H452-H457 ◽  
Author(s):  
F. M. Siri
Keyword(s):  
Heart Rate ◽  
Cardiac Hypertrophy ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Time Course ◽  
Plasma Catecholamines ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Norepinephrine Turnover

Cardiac hypertrophy is frequently associated with sympathetic changes that include increased myocardial norepinephrine turnover, depleted myocardial norepinephrine stores, decreased myocardial responses to sympathetic nerve stimulation, and elevated plasma catecholamines. To better understand these events mechanistically, the time course of each was assessed in rat hearts subjected to aortic constriction-induced pressure overload. There was no evidence of increased left ventricular norepinephrine turnover in abdominal aortic-constricted rats, when compared with sham-constricted animals, during the first 3 days postoperatively. Moreover, their turnover rate constants tended to be lower during this period, then increased significantly by day 7. Plasma catecholamines were increased and left ventricular norepinephrine stores were decreased only on day 7. Heart rate responses to maximal sympathetic nerve stimulation were significantly reduced on the third postoperative day. Thus the decrease in norepinephrine stores coincided with changes in left ventricular norepinephrine turnover and plasma catecholamines, whereas the reduction in heart rate responses did not. This pattern suggests an initial reflex decrease in myocardial sympathetic tone, followed by baroreceptor resetting, with an eventual increase in general sympathetic outflow. The period of increasing catecholamine stimulation occurred after a relative left ventricular hypertrophy had developed but before a significant increase in absolute left ventricular mass. Thus catecholamines may still importantly contribute to the hypertrophy seen in this model.

Intermittent hypoxia modulates nNOS expression and heart rate response to sympathetic nerve stimulation

2001 ◽  
Vol 281 (1) ◽  
pp. H132-H138 ◽  
Author(s):  
R. M. Mohan ◽  
S. Golding ◽  
D. J. Paterson
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Intermittent Hypoxia ◽  
Stellate Ganglion ◽  
No Synthase ◽  
Sympathetic Nerve Stimulation ◽  
Synthase Inhibitor ◽  
The Right ◽  
And Control

Nitric oxide (NO) decreases norepinephrine (NE) release and the heart rate (HR) response to sympathetic nerve stimulation (SNS). We tested the hypothesis that the enhanced HR response to sympathetic activation following chronic intermittent hypoxia (IH) results from a peripheral modulation of pacemaking by NO. Isolated guinea pig double atrial/right stellate ganglion preparations were studied from animals that had been exposed to IH ( n = 20) and control animals ( n = 22). The HR response to SNS was significantly enhanced in the IH group compared with the controls. However, the increase in HR with cumulative doses (0.1–10 μM) of bath-applied NE was similar in both groups. Western blot analysis showed less neuronal NO synthase in the right atria from the IH group. In IH animals, the NO synthase inhibitor, N ω-nitro-l-arginine (l-NNA; 100 μM) did not alter the increased HR response to SNS, whereas in control animals l-NNA significantly increased the HR response to SNS; an effect that was reversed with excess l-arginine. In conclusion, the enhanced HR response to SNS after IH may be related to a decreased inhibitory action of NO on presynaptic NE release.

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses of atrium and ventricle to sustained sympathetic nerve stimulation

1991 ◽  
Vol 261 (6) ◽  
pp. H1889-H1894
Author(s):  
M. Furuyama ◽  
T. Haneda ◽  
J. Ikeda ◽  
T. Hiramoto ◽  
T. Sakuma ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Stellate Ganglion ◽  
Left Ventricular ◽  
Right Atrial ◽  
Control Group ◽  
Inotropic Response ◽  
Sympathetic Nerve Stimulation ◽  
Chronotropic Response ◽  
Control Value

To determine whether chronotropic and atrial inotropic responses to sympathetic nerve stimulation are maintained longer than ventricular inotropic response, the present study was performed with control and acute reserpinized dogs. We stimulated the right stellate ganglion of both groups supramaximally for 60 min and compared right atrial responses (chronotropism and inotropism) with left ventricular (LV) dP/dtmax. In the control group, heart rate (HR) immediately increased and was only slightly attenuated with 60 min of stimulation, and right atrial (RA) inotropic response was less attenuated than was LV response (7% in HR, 33% in RA dP/dtmax, 50% in LV dP/dtmax, P less than 0.01, from the peak value of each response). RA and LV norepinephrine (NE) content was decreased by the stimulation but remained higher than the LV control value. In the reserpinized group, NE content in the RA was low before the stimulation and was further decreased by the stimulation. In this group, HR response was attenuated (27% in HR, P less than 0.01) as was LV dP/dtmax, and the difference in contractile responsiveness between atrium and ventricle disappeared (58% in RA dP/dtmax vs. 61% in LV dP/dtmax, NS). The results indicate that the chronotropic response was only slightly attenuated and that the atrial contractile response was attenuated less than the ventricular response, with sustained sympathetic nerve stimulation in the normal heart. This can be ascribed to the much higher NE content in the RA than that in the LV.

Alpha-adrenergic vasoconstriction in normal and hypoperfused myocardium during sympathetic nerve stimulation

1992 ◽  
Vol 263 (6) ◽  
pp. H1682-H1688 ◽  
Author(s):  
J. Westby ◽  
S. Birkeland ◽  
S. E. Rynning ◽  
O. L. Myking ◽  
J. Lekven ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Adrenergic Receptors ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Coronary Perfusion ◽  
Sympathetic Nerve Stimulation

Coronary vasoconstriction mediated by postjunctional alpha 1- and alpha 2-adrenergic receptors was studied in normally perfused (control group) and left coronary hypoperfused (stenosis group) hearts of vagotomized, beta-blocked (propranolol) cats. Cardiac sympathetic nerve stimulation was combined with alpha 1- and subsequent alpha 2-adrenergic antagonism (doxazosin and SK &F 104078). Coronary perfusion pressure and heart rate were kept constant within groups; regional myocardial blood flow and cardiac output were obtained by means of microspheres with concomitant measurement of left ventricular myocardial oxygen consumption (MVO2). alpha 1-Adrenergic antagonism alone did not significantly alter blood flow in any wall layer in either group. Subsequent alpha 2-adrenergic antagonism increased epicardial as well as composite transmural flow in the stenosis group (P < 0.025). The inverse correlation between coronary resistance and MVO2 vanished in the stenosis group following alpha 1- and alpha 2-adrenergic antagonism. Maximal first derivative of the left ventricular pressure-time relation (dP/dt) and cardiac output were reduced simultaneously (P < 0.001). Hence, the significance of alpha 1- and alpha 2-adrenergic stimulation of inotropy and cardiac performance are augmented by myocardial hypoperfusion. Furthermore, alpha 2-adrenergic receptors are responsible for epicardial vasoconstriction in hypoperfused myocardium.

Effects of hydralazine on blood pressure, pressor mechanisms, and cardiac hypertrophy in two-kidney, one-clip hypertensive rats

1986 ◽  
Vol 64 (12) ◽  
pp. 1528-1534 ◽  
Author(s):  
James Tsoporis ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Time Course ◽  
Antihypertensive Effect ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Prolonged Treatment ◽  
Internal Diameter ◽  
Hypertensive Rats ◽  
Blood Volumes

In 2-kidney, 1-clip hypertensive rats, the time course of changes in blood pressure (BP), heart rate, activity of the sympathetic nervous system and the renin–angiotensin system, plasma and blood volumes, left ventricular (LV) and right ventricular (RV) weight, and LV dimensions were evaluated during treatment with hydralazine 80 and 120 mg/L drinking water for 2 days or 1, 2, 3, 5, and 8 weeks. Hydralazine induced initially a clear antihypertensive effect (mean BP from 170–180 down to 135–145 mmHg (1 mmHg = 133.32 Pa)), subsequently tolerance developed. Heart rate, plasma catecholamines, and the blood pressure response to hexamethonium were not affected by treatment. Significant increases in plasma renin activity occurred during the initial 1–3 weeks of treatment. Plasma and blood volumes showed only small increases with prolonged treatment. RV weight and LV internal diameter showed significant increases at 3, 5, and 8 weeks of treatment, LV weight at 5 and 8 weeks. LV wall thickness did not change significantly. Thus, treatment with the arterial vasodilator hydralazine causes both RV hypertrophy and eccentric LV hypertrophy. Intravascular volume expansion, associated possibly with redistribution of blood volume to the central compartment, may play a major role in these cardiac effects. Increased renin release but not a generalized increase in sympathetic tone may play a role in the development of tolerance to the antihypertensive effect.

Sign in / Sign up

Export Citation Format

Share Document