Myocardial Hypertrophy Produced by Chronic Infusion of Subhypertensive Doses of Norepinephrine in the Dog

Laks, Michael M.; Morady, Fred; Swan, H.J.C.

doi:10.1378/chest.64.1.75

Cited by 250 publications

(71 citation statements)

References 22 publications

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“…17 A number of clinical and experimental studies have demonstrated a close relationship between the level of adrenergic activity and the development of left ventricular hypertrophy. [14][15][16][17] Catecholamines play an important role in the devel-opment and maintenance of left ventricular hypertrophy. Noradrenaline is implicated in the development of left ventricular hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Mild chronic renal insufficiency induces sympathetic overactivity

Tinucci

et al. 2001

J Hum Hypertens

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The objectives of this study were to evaluate baseline sympathetic nerve activity as well as the mechanisms of sympathetic overactivity in mild chronic renal insufficiency hypertension. Seven hypertensives with mild renal insufficiency, seven hypertensives with normal renal function and seven normotensives, age and weight-matched were studied on one session to evaluate baseline muscle sympathetic nerve activity measured in the peroneal nerve. The mild renal insufficiency hypertensives and the hypertensives with normal renal function were also studied to evaluate arterial baroreflex control of muscle sympathetic nerve activity assessed by increasing and decreasing blood pressure through continuous infusion of phenylephrine and sodium nitroprusside respectively. Baseline muscle sympathetic nerve activity was significantly higher in mild renal insufficiency hypertensives (34 bursts/min) when com-

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Section: Discussionmentioning

confidence: 99%

Mild chronic renal insufficiency induces sympathetic overactivity

Tinucci

et al. 2001

J Hum Hypertens

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“…An initial study 21 in 1971 described a dose-response curve to NE in which progressive increases in NE delivery resulted in increases in HR, blood pressure, cardiac output and total peripheral resistance. A later study by these authors 22 examined the effects of prolonged (6-63 weeks) NE infusion. A dose for infusion was chosen that did not produce hypertension.…”

Section: Discussionmentioning

confidence: 99%

Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs.

King¹,

Sack²,

Kichuk³

et al. 1987

Hypertension

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SUMMARY To better define the mechanisms of blood pressure control in states of catecholamine excess, we infused norepinephrine for 28 days using subcutaneously implanted osmotic pumps in dogs previously instrumented for monitoring left ventricular dynamics and cardiac output. Plasma norepinephrine rose from 238 ± 27 to 4346 ± 952 pg/ml at 21 days, while epinephrine and dopamine levels did not change. Heart rate fell from 85 ± 4 to 63 ± 6 beats/min, while arterial pressure was unchanged from baseline. Total peripheral resistance rose 0.011 ± 0.003 mm Hg/ml/min from a control value of 0.029 ± 0.002 mm Hg/ml/min, and cardiac output decreased 1093 ± 292 ml/min from a baseline level of 3575 ± 156 ml/min. Since stroke volume did not change, the maintenance of arterial pressure is related to decreases in cardiac output secondary to bradycardia. Buffering mechanisms are responsible for maintenance of systemic arterial pressure because hexamethonium and atropine caused hypertension. Although left ventricular end-diastolic pressure, end-diastolic diameter, shortening, rate of change of pressure, velocity of myocardial shortening, cardiac work, stroke work, and the double product did not change significantly during the study, postmortem examination demonstrated biventricular hypertrophy. Thus, despite markedly elevated catecholamine levels and no elevation of systemic arterial pressure, myocardial hypertrophy developed. These studies lend support to the hypothesis that norepinephrine may be a direct myocardial tropic hormone and suggest that intense activation of reflex buffering mechanisms maintains blood pressure in the normal range during chronic catecholamine infusion. (Hypertension 9: 582-590, 1987) KEY WORDS • bradycardia • hypertension • hypertrophy • catecholamines • total peripheral resistance • atropine E LEVATIONS in catecholamine levels may be associated with a number of disease states, including mitral valve prolapse (MVP), 1 -2 chronic myocardial failure, 3 " 6 and pheochromocytoma. 7 These disease states may be characterized by sustained or episodic hypertension, myocardial dysfunction, and cardiomyopathy.Recently, it has been noted that certain patients with MVP, chronic myocardial failure, or pheochromocytoma have dysautonomia, manifested by abnormalities in heart rate or blood pressure response (or both) to orthostatic change or exercise. 8 " 12 Some investigations of patients with MVP having dysautonomia are consistent with evidence of hyperadrenergic states and some with simultaneous hypervagatonia. 9 -13 Significant elevations in serum catecholamine levels have been observed in a group of symptomatic patients with MVP 1 ' l4 ; these results have been confirmed by other workers. 2 ' 8> l5 Patients with chronic myocardial failure, regardless of etiology, have elevated plasma norepinephrine (NE) levels. 16 In addition, defects in baroreceptor reflex-mediated vasoconstrictor responses have been noted in dogs 17 and in patients 18 -19 with marked myocardial dysfunction.Several studies, summarized by Ec...

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“…Studies in experimental animals have suggested a possible link between cardiac hypertrophy and the sympathetic system. Experimentally, chronic nonhypertensive infusion of noradrenaline in dogs caused cardiac hypertrophy simulating hypertrophic cardiomyopathy (Blaufuss et al, 1975;Laks et al, 1973). The adrenergic system of the ventricular septum was initially different and responded differently to norepinephrine infusion over 3 months compared with that of the right and left ventricles before development of hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

“…Recently it has been reported that the response of blood norepinephrine to postural change and cold pressor test is abnormal in patients with HCM ). An experimental study demonstrated that nonhypertensive infusion of norepinephrine into dogs introduced left ventricular hypertrophy (Laks et al, 1973) simulating hypertrophic obstructive cardiomyopathy (Blaufuss et al, 1975). These studies suggest that sympathetic abnormality exists in ASH and that it can influence cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

Difference in the response to isoproterenol between asymmetric septal hypertrophy and symmetric hypertrophy in patients with hypertrophic cardiomyopathy

Iida

Sugishita

Matsuda

et al. 1986

Clinical Cardiology

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Summary:The response to isoproterenol was studied in 9 patients with hypertrophic cardiomyopathy (HCM) and asymmetric septal hypertrophy (ASH), 9 patients with HCM and symmetric hypertrophy (SH), and 9 normal controls (NC), using digitized M-mode echocardiography. There was no significant difference in fractional shortening (FS) between ASH and SH, nor between SH and NC before isoproterenol infusion. During isoproterenol infusion, however, FS was significantly greater in ASH (60f6%) than in SH (53f7%) and NC (49f5%) (p

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Myocardial Hypertrophy Produced by Chronic Infusion of Subhypertensive Doses of Norepinephrine in the Dog

Cited by 250 publications

References 22 publications

Mild chronic renal insufficiency induces sympathetic overactivity

Mild chronic renal insufficiency induces sympathetic overactivity

Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs.

Difference in the response to isoproterenol between asymmetric septal hypertrophy and symmetric hypertrophy in patients with hypertrophic cardiomyopathy

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