Participation of endogenous catecholamines in the regulation of left ventricular mass in progeny of hypertensive parents.

Trimarcö, Bruno; Ricciardelli, Bruno; Luca, Nicola De; Simone, Antonio De; Cuocolo, A.; Galva, M. D.; Picotti, G. B.; Condorelli, M

doi:10.1161/01.cir.72.1.38

Cited by 50 publications

(15 citation statements)

References 44 publications

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“…Finally, a recent report front our labora tory [26] has indicated that endogenous catecholamines physiologically regulate LV mass in a hypertensive prog eny, thus confirming the indirect evidence that the sym pathetic system may be involved in the control of LV mass.…”

Section: Cardiac Hypertrophy In Human Hypertensionsupporting

confidence: 59%

Reversal of Left Ventricular Hypertrophy following Treatment with Beta-Blockers: Experience with Tertatolol

Trimarco¹,

Ricciardelli²,

Luca³

et al. 1986

Am J Nephrol

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Hypertrophy in response to increasing blood pressure in primary hypertension leads to important functional consequences for the left ventricle. In fact, the progression of hypertensive heart disease, from an adaptive left ventricular hypertrophy with compensated ventricular function to severe hypertrophy with left ventricular failure, has been long thought to be related to the severity and duration of hypertension. Antihypertensive treatment seems to prevent or minimize the occurrence of left ventricular hypertrophy, but questions arise as to whether this therapy is also able to restore normal hemodynamic conditions, or at least to minimize the hemodynamic abnormalities. This review aims at summarizing current knowledge on the effects of the antihypertensive treatment with β-blockers, including tertatolol, on hypertension-induced left ventricular hypertrophy. The pathogenetic mechanisms underlying the cardiovascular changes associated with hypertension are discussed. A decrease in left ventricular wall thickness as well as in left ventricular mass has been reported in most of the studies performed with different types of β-adrenergic blocking agents. The extent of this reduction seems to be related not only to the fall in systemic blood pressure, but also to a decrease in sympathetic stimulation. With regard to the functional consequences of hypertension, the reversal of left ventricular hypertrophy following antihypertensive treatment with β-blockers is usually associated with an improvement in left ventricular performance. This phenomenon can hardly be ascribed to the direct effects of β-blocking agents. It is more likely to be related to the concomitant reduction in the afterload and to the improved left ventricular compliance, associated with a decrease in left ventricular wall thickness.

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Section: Cardiac Hypertrophy In Human Hypertensionsupporting

confidence: 59%

Reversal of Left Ventricular Hypertrophy following Treatment with Beta-Blockers: Experience with Tertatolol

Trimarco¹,

Ricciardelli²,

Luca³

et al. 1986

Am J Nephrol

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“…Two-dimensional and M-mode echocardiograms were obtained and processed as previously reported from this laboratory. 14 Two days before the invasive study session, the subjects were made familiar with the LBNP device and the neck chamber. Subjects were requested to refrain from cigarette smoking and coffee drinking during the 12 hours immediately prior to the study session.…”

Section: Methodsmentioning

confidence: 99%

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

et al. 1987

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SUMMARY The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 ± 0.1 to 2.0 ± 0.1 pg/ml; p<0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors. (Hypertension 10: 595-602, 1987) KEY WORDS • propranolol • lower body negative pressure • norepinephrine A LTHOUGH the sensitivity of the nonosmotic / \ control of arginine vasopressin (AVP) release A. JL. in humans seems to be somewhat controversial, 1 " 4 recent reports 5 ' 6 support the hypothesis that factors other than blood osmolarity are involved in the regulation of AVP release in humans. In particular, Leimbach et al. 5 demonstrated that combined unloading of cardiac and arterial baroreceptors induced by lower body negative pressure (LBNP) increases plasma AVP in subjects with high plasma osmolality. Egan et al. 6 reported that the selective unloading of cardiopulmonary receptors, by thigh-cuff inflation, increases plasma AVP levels in humans. These observations raise the possibility that AVP release may be altered in patients with impaired cardiopulmonary or arterial baroreceptor reflex responsiveness.From the Istituto di Clinica Medica I, II Facolta di Medicina e Chirurgia, Universita di Napoli, Italy.Address for reprints: Bruno Trimarco, M.D., Istituto di Clinica Medica I, II Facolta di Medicina, via S. Pansini 5, 80131 Napoli, Italy.Received November 4, 1986; accepted June 30, 1987. In patients with established hypertension, we observed that the postural change from the supine to the upright position did not induce the rise in AVP plasma levels observed in normote...

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“…We did not test whether NE was the proximate stimulus for the mRNA changes with aortic banding, but sympathetic activity is increased in animals and humans with hypertrophy (for examples see Refs. [42][43][44][45].…”

Section: Figmentioning

confidence: 99%

α1-Adrenergic Receptor Subtype mRNAs Are Differentially Regulated by α1-Adrenergic and Other Hypertrophic Stimuli in Cardiac Myocytes in Culture and In Vivo

Rokosh

Stewart

Chang

et al. 1996

Journal of Biological Chemistry

155

118

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The three cloned ␣ 1 -adrenergic receptor (AR) subtypes, ␣ 1B , ␣ 1C , and ␣ 1D , can all couple to the same effector, phospholipase C, and the reason(s) for conservation of multiple subtypes remain uncertain. All three ␣ 1 -ARs are expressed natively in cultured neonatal rat cardiac myocytes, where chronic exposure to the agonist catecholamine norepinephrine (NE) induces hypertrophic growth and gene transcription. We show here, using RNase protection, that the ␣ 1 -AR subtype mRNAs respond in distinctly different ways during prolonged NE exposure (12-72 h). ␣ 1B and ␣ 1D mRNA levels were repressed by NE, whereas ␣ 1C mRNA was induced. Changes in mRNA levels were mediated by an ␣ 1 -AR, were not explained by altered mRNA stability, and were reflected in receptor proteins by [ 3 H]prazosin binding. ␣ 1 -AR-stimulated phosphoinositide hydrolysis and myocyte growth were not desensitized. Three other hypertrophic agonists in culture, endothelin-1, PGF2␣, and phorbol 12-myristate 13-acetate, also induced ␣ 1C mRNA and repressed ␣ 1B mRNA. In myocytes from hearts with pressure overload hypertrophy, ␣ 1 mRNA changes were identical to those produced by NE in culture. These results provide the first example of a difference in regulation among ␣ 1 -AR subtypes expressed natively in the same cell. Transcriptional induction of the ␣ 1C -AR could be a mechanism for sustained growth signaling through this receptor and is a common feature of a hypertrophic phenotype in cardiac myocytes. The natural catecholamines norepinephrine (NE)1 and epinephrine activate adrenergic receptors (ARs) in three families, ␣ 1 , ␣ 2 , and ␤. Multiple subtypes have been cloned within each family: three ␣ 1 -ARs (B, C, and D), 2 three ␣ 2 -ARs (A, B, and C; also called C10, C2, and C4, respectively), and three ␤-ARs (1, 2, and 3) (1). The reason(s) for conservation of multiple subtypes remain uncertain, since all subtypes in each family couple preferentially to the same effector when overexpressed, ␣ 1 -ARs to activation of phospholipase C (PLC), ␣ 2 -ARs to inhibition of adenylyl cyclase, and ␤-ARs to activation of adenylyl cyclase (1). An intriguing difference among ␤-AR and ␣ 2 -AR subtypes has been suggested recently, in the regulation of receptor levels during prolonged agonist exposure. Levels of the ␤ 3 -AR (2-4) and the ␣ 2C -AR (5, 6) are not down-regulated during long term agonist exposure, at least in some cells, in contrast with downregulation of ␤ 1 -and ␤ 2 -ARs, and ␣ 2A -and ␣ 2B -ARs. Downregulation of receptor expression is thought to be a major determinant of desensitization when catecholamine exposure is prolonged (7). Conversely, a receptor that is induced by agonist might be adapted to mediate catecholamine responses when sympathetic activity is increased chronically, a condition that occurs frequently in the intact organism.We have been studying a physiological response that develops over long periods of catecholamine exposure, ␣ 1 -adrenergic induction of hypertrophic growth and gene transcription in primary cultures of neon...

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Participation of endogenous catecholamines in the regulation of left ventricular mass in progeny of hypertensive parents.

Cited by 50 publications

References 44 publications

Reversal of Left Ventricular Hypertrophy following Treatment with Beta-Blockers: Experience with Tertatolol

Reversal of Left Ventricular Hypertrophy following Treatment with Beta-Blockers: Experience with Tertatolol

Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy.

α1-Adrenergic Receptor Subtype mRNAs Are Differentially Regulated by α1-Adrenergic and Other Hypertrophic Stimuli in Cardiac Myocytes in Culture and In Vivo

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