Effect of stress and sympathetic activity on rat cardiac and aortic ornithine decarboxylase activity

Thadani, Pushpa V.; Schanberg, Saul M.

doi:10.1016/0024-3205(79)90585-x

Cited by 25 publications

(11 citation statements)

References 13 publications

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“…These results demonstrated that betaadrenoceptor stimulation activated protein synthesis of cultured vascular smooth muscle cells similarly to its activation of ODC activity in rat myocardial cells in vivo. 18 In contrast to our findings under tissue culture conditions free from the effect of blood pressure, Thadani et al 19 reported that the sympathetic regulation of ODC activity levels is mediated through alpha-receptor in the rat aorta in vivo. ODC activation by alphastimulation in vivo may be due to blood pressure elevation.…”

Section: Effect Of Phosphodiesterase Inhibitor and A Cyclic Amp Analogcontrasting

confidence: 55%

Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats.

Kanbe¹,

Nara²,

Tagami³

et al. 1983

Hypertension

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SUMMARY Mechanisms of vascular hypertrophy induced by hypertension were studied in cultured aortic smooth muscle cells from spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) and compared with those from normotensive Wistar-Kyoto (WKY) rats. Fetal calf serumstimulated ornithine decarboxylase (ODC) activity of cultured smooth muscle cells was greater in SHR and SHRSP than in WKY. Beta-but not alpha-adrenergic agonist stimulated ODC activity acutely in cultured smooth muscle cells from WKY, and isoprenaline-induced activation was blocked by the beta-blocker, propranolol, and enhanced by the phosphodiesterase inhibitor, l-methyl-3-isobutylxanthine. These results indicate that cultured vascular smooth muscle cells from SHR and SHRSP are more prone to increase the protein synthesis than those from WKY through the trophic induction of ODC activity and that the regulation of ODC activity by catecholamines is mediated through betaagonistic effect in cultured smooth muscle cells. (Hypertension 5: 887-892, 1983) KEY WORDS • catecholamine * cultured vascular smooth muscle cells ornithine decarboxylase * stroke-prone spontaneously hypertensive rats spontaneous hypertension I T is now established that functional as well as structural vascular changes are important in the pathogenesis of genetic hypertension. Medial hypertrophy of arterial walls is generally regarded as being secondary to blood pressure rise but involved in the further development and maintenance of hypertension.' However, in spontaneously hypertensive rats (SHR), the thickening of the arterial walls is induced at the early stage or prehypertensive stage of hypertension. "7 Furthermore, we found that vascular noncollagen and collagen protein synthesis was enhanced not only by the blood pressure rise itself but also by genetic predisposition and neural activation, 8 and that vascular hypertrophy in SHR was prevented by the prolonged treatment of a low dose of beta-blocker which did not obviously affect blood pressure. 9Under tissue culture condition free from the influence of blood pressure, smooth muscle cells from SHR and stroke-prone SHR (SHRSP) grew faster than those from normotensive Wistar-Kyoto (WKY) rats, and la-

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Section: Effect Of Phosphodiesterase Inhibitor and A Cyclic Amp Analogcontrasting

confidence: 55%

Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats.

Kanbe¹,

Nara²,

Tagami³

et al. 1983

Hypertension

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“…M e a n * SEM -R V -L V increase in LV ODC specific activity as had been previously suggested (3,25). Neither d o endogenous catecholamines appear to rise in the rabbit myocardium until 7 days (8) suggesting that the endogenous release of catecholamines may not induce LV O D C activity.…”

Section: Discussionsupporting

confidence: 69%

“…It has been recently suggested that an increase in either circulating and/or endogenous catecholamines may activate ODC in the rat heart (3,25). ODC activity in these reports was determined in the whole heart; however, because this study has shown that RV ODC did not increase at day 1 or 2 it is unlikely that circulating factors such as catecholamines initiate the observed free wall were expressed as a function of age in this figure.…”

Section: Discussionmentioning

confidence: 83%

Polyamine Metabolism during the Perinatal Development of the Rabbit Right and Left Ventricle

Boucek

Davidson

1982

Pediatr Res

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Summary cardiovascular alterations (19) is accom~anied bv increased mvo-The right ventricular (RV) and left ventricular (LV) free wall weights, ornithine decarboxylase (ODC) specific activity and polyamine content were determined in fetal, I-, 2-, 7-, 14, and 21-day-old rabbit hearts. There was a significant increase in the LV free wall weight and a decrease in RV free wall weight between 1-7 days. By day 7 the LV/RV mass ratio doubled and reached a ratio comparable to that seen in adult rabbit hearts. The rate of change in the LV and RV free wall weights were comparable after day 7.There was a significant increase in LV ODC specific activity and a decrease in RV ODC specific activity after birth. The LV ODC specific activity was significantly greater than RV ODC specific activity in both 1 and 2 day old rabbit hearts whereas they were not significantly different in 7 and 14 day old rabbit hearts.The molar content (nmoles/mg wet weight or nmoles/mg protein) of putrescine decreased approximately Ifold fter birth in the RV but increased approximately 2-fold in the LV. The molar content of spermidine and spermine was transiently increased after birth (1 day old) in both RV and LV with approximately a 2-fold increase in spermidine and a 2.5-fold (LV) and 4-fold (RV) increase in spermine content. The increase in LV putrescine content after birth was due, at least in part, to the observed increase in ODC specific activity in the LV free wall. The putrescine/spermidine ratio increased in the LV and decreased in the RV immediately after birth up to day 7. As opposed to the shortlived increase in spermidine and spermine observed in both the RV and the LV free wall, increased ODC specific activity and putrescine accumulation uniquely characterized the preferential growth of the LV between day 1 and 7.cardial cell number as well as increased cell sizi(l0). In the hrst wk of postnatal life an increase in myocyte number accounts for the 2-fold weight difference between the left and right ventricles for developing rats (2).Other differences also have been observed in the rate of microvascular and subcellular organelle maturation of the left versus right ventricle (16,23). From the morphologic features of the neonatal rat heart, LV growth is analogous to combined eccentric and concentric hypertrophy whereas right ventricular growth is analagous to eccentric hypertrophy (2). Presumably the postnatal pressure loading of the newborn LV accelerates its rate of growth with features similar to concentric hypertrophy due to pressure overloading in pathologic states. Thus the postnatally developing heart affords an ideal model for studying the relationship between pressure loading and adaptive myocardial growth because paired comparisons of left and right ventricular parameters are possible.An increase in ornithine decarboxylase (EC. 4.1.1.17) activity, and increased polyamine production by this enzyme, occurs during the initiation of adaptive myocardial growth in the pressure overloaded adult heart. Acute banding experiments have dem...

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“…A 4-hour time interval was chosen because this is when ODC levels have been found to be maximally induced after aradrenergic receptor agonist administration in the aorta. 16 Methoxamine (2,5, or 10 mg/kg of 10 mg/ml methoxamine solution in saline) or control (saline, 1.0 ml/kg of 0.9% NaCl [wt/vol] in distilled water) treatment was administered subcutaneously between 9 AM and noon. Direct measurements of MAP were recorded in conscious rats previously implanted with aortic catheters, as described below; after 4 hours, the rats were killed by anesthetic overdose (sodium pentobarbital, 60 mg/kg i.p.)…”

Section: Treatmentmentioning

confidence: 99%

“…Previous reports have shown that enormous doses of hydralazine (two to four times the largest dose used in the present study) induced cardiac ODC activity, as well as a modest aortic activation, by way of reflex mechanisms. 16 Unfortunately, that study did not assess cardiac sympathetic activity, not even indirectly by measuring HR.…”

mentioning

confidence: 99%

Vasodilators inhibit acute alpha 1-adrenergic receptor-induced trophic responses in the vasculature.

1992

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Cardiovascular hypertrophy plays an important role in the development and maintenance of hypertension. Hyperactivity of the sympathetic nervous system may be one of the initiating factors responsible for the stimulation of growth processes involved in these structural alterations. We have used a wellestablished early biochemical marker of cellular growth processes, induction of ornithine decarboxylase (ODC), to determine whether «,-adrenergic receptor-induced vascular trophic responses are dependent on arterial pressure elevation. Hydralazine or felodipine were coadministered to control the 0,-adrenergjc receptor agonist-induced rise in mean arterial pressure (MAP). Methoxamine is marked hypertrophy of the heart and resistance vessels constituting a physiological structural adaptation. -2 Folkow and colleagues 34 were the first to demonstrate that vascular structural changes, manifested as an increase in the wall thickness and a consequent decrease in the lumen diameter, were critical alterations in the maintenance of an elevated arterial pressure.Besides an augmented arterial pressure, trophic mechanisms have been postulated to lead to the development of cardiac and vascular hypertrophy by means of hyperactivity of neuroendocrine systems. The sympathetic nervous system represents one system in particular that has received substantial attention as an initi-

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Effect of stress and sympathetic activity on rat cardiac and aortic ornithine decarboxylase activity

Cited by 25 publications

References 13 publications

Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats.

Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats.

Polyamine Metabolism during the Perinatal Development of the Rabbit Right and Left Ventricle

Vasodilators inhibit acute alpha 1-adrenergic receptor-induced trophic responses in the vasculature.

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