Changes in renal vascular reactivity at various stages of deoxycorticosterone hypertension in rats.

Berecek, Kathleen H.; Stocker, M; Gross, F.

doi:10.1161/01.res.46.5.619

Cited by 83 publications

(42 citation statements)

References 24 publications

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“…However, it is not known how long maternal glucocorticoids need to be elevated before causing irreversible postnatal effects. Although we found that plasma renin and angiotensin II concentrations were unchanged with cortisol infusion, previous investigators have shown that glucocorticoids may increase vascular sensitivity to vasoconstrictors such as angiotensin II and catecholamines in the fetus and adult (Berecek et al 1980, Tangalakis et al 1992, Whitworth et al 1995.…”

Section: Blood Pressurecontrasting

confidence: 66%

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Jensen¹,

Gallaher²,

Breier³

et al. 2002

Journal of Endocrinology

114

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Exposure of the fetus to excess maternal glucocorticoids has been postulated to alter fetal growth and development, and thus provide a possible mechanism for the link between impaired fetal growth and altered postnatal physiology. However, the effects of exposure to excess maternal glucocorticoids on fetal physiology and metabolism in utero have not been described. We therefore studied the effects of chronic maternal cortisol infusion on fetal growth, blood pressure, metabolism and endocrine status in chronically catheterised fetal sheep. We infused hydrocortisone (80 mg/day, n=6) or saline (n=8) for 10 days into the pregnant ewes beginning at 119 days of gestation. Maternal cortisol infusion reduced fetal growth rate by 30% (girth increment 2·9 0·3 vs 1·8 0·4 mm/ day, P=0·03). Maternal cortisol infusion increased fetal heart weight by 15% relative to body weight and increased ventricular wall thickness by 30% in the left and 50% in the right ventricle. The weight of the spleen was reduced by 30% and placental weight reduced by 25%. Fetal blood pressure increased by approximately 10 mmHg (20%) during maternal cortisol infusion.Maternal cortisol infusion did not alter amino-nitrogen concentrations. However, maternal lactate concentrations increased by 80% and fetal lactate concentrations increased by 74% with maternal cortisol infusion, and both maternal and fetal urea concentrations increased by 40%. Circulating maternal IGF-binding protein (IGFBP)-3 levels had increased by 20% by the end of the maternal cortisol infusion. Fetal IGF-I concentrations decreased during cortisol infusion and fetal IGFBP-1 concentrations were negatively correlated with fetal weight (r= 0·76, P=0·02).We conclude that even a modest elevation of maternal cortisol levels affects fetal growth, cardiovascular function, metabolism and endocrine status which may have longterm consequences.

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Section: Blood Pressurecontrasting

confidence: 66%

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Jensen¹,

Gallaher²,

Breier³

et al. 2002

Journal of Endocrinology

114

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“…The responses to neurotransmitters have been extensively studied but the overall picture is unclear. Results of experiments using intact animals or vascular beds suggest that noradrenaline sensitivity is greater in spontaneously hypertensive rats (SHR) than in Wistar Kyoto (WKY) controls (Lais et al, 1974;Berecek et al, 1980). Experiments using isolated preparations suggest that it is only part of the SH vasculature which shows increased sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Abnormal vascular phosphoinositide hydrolysis in the spontaneously hypertensive rat

Heagerty

Ollerenshaw

Swales

1986

British J Pharmacology

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1 The production of [3H]-inositol phosphates was studied in labelled segments of aorta from spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) controls at 5 and 19 weeks, either unstimulated or in the presence of noradrenaline. 2 Basal hydrolysis of inositol phospholipids was significantly enhanced in young SHR (P < 0.05) compared to controls but this difference was no longer detected at 19 weeks. 3 Noradrenaline increased [3H]-inositol phosphate accumulation in both SHR and WKY, but maximal hydrolysis was significantly greater in WKY (P <0.01), although the ED50 was similar in both groups of animals. 4 These data demonstrate that phosphatidylinositide hydrolysis is enhanced in the young hypertensive rat at the time blood pressure is rising, but that this activity has declined by the time hypertension has reached an established phase. In addition, a,-agonist induction of inositol phospholipid hydrolysis differs in the two species of animals, being reduced in genetically mature hypertensive rats.

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“…Observations in the steroid hypertensive dog of : 1) a diminished circulating catecholamine level (Bravo et al 1977), 2) suppressed carotid occlusion reflex (Ueno et al 1988), and 3) normal BP and iliac vascular resistance response to a-adrenoceptor blockade (Zeigler and Zimmerman 1987) had earlier made this point. It might even be postulated that tonic sympathetic nerve activity is subnormal in the DOCA-salt hypertensive dog, since vascular reactivity to norepinephrine is actually increased (Berecek et al 1980 ;Goering et al 1988), and as a result one would expect greater tonically mediated renal adrenergic vasoconstriction even in the presence of normal sympathetic nerve activity. These results are in marked contrast to the substantial evidence for the role of the sympathetic nervous system in DOCA-salt hypertension in the rat.…”

Section: Resultsmentioning

confidence: 99%

“…Because there is evidence of enhanced renal adrenergic vascular reactivity (Berecek et al 1980; Goering et al 1988) and adrenergic vascular tone (Ciccone and Zambraski 1986) in DOCA-salt hypertension in several species, we sought to determine whether there is an adrenergic influence on renal hemodynamics in the DOCA-salt hypertensive dog.…”

mentioning

confidence: 99%

Renal Hemodynamics in Canine DOCA-Salt Hypertension: Effect of Calcium Channel Blockade.

Zimmerman

Raich

1992

Tohoku J. Exp. Med.

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Systemic arterial blood pressure (BP), renal blood flow (RBF), and renal vascular resistance (RVR) were followed for 3-4 wks during the progression of DOCA-salt hypertension in the conscious dog. Accompanying the gradual increase in BP was an increase in RBF ; however, RVR was unchanged. The hypertension was totally reversed 5-7 days after cessation of DOCA-salt treatment, but the increase in RBF persisted, presumably as a result of renal hypertrophy. Renal adrenoceptor blockade with prazosin (6 dogs) and prazosin plus idazoxan (4 dogs) caused a comparable decrease in BP in the normotensive and DOCA-salt hypertensive dog ; however, RVR was decreased only in the normotensive. Similar results were obtained during ganglionic blockade with hexamethonium. The i.v. infusion of diltiazem for 1 wk restored BP of the hypertensive dog to a normotensive level, and hexamethonium given i.v. had little further effect on either BP or RVR. These results suggest a non-neurogenically mediated mechanism of canine DOCA-salt hypertension that is susceptible to calcium channel blockade, calcium channel blockers ; hypertension ; desoxycorticosterone ; renal blood flow ; renal hemodynamics Desoxycorticosterone acetate-salt hypertension has been studied intensively for many years, using the rat model. The consensus is that the sympathetic nervous system plays an integral role in the etiology of this form of hypertension in the rat (DeChamplain et al. 1969;Takeda and Bunag 1980;Koepke et al. 1986). Increased basal sympathetic vascular tone as well as enhanced sympathetic activity during stress are believed to contribute to the hypertension. More recently, evidence has been presented for involvement of the central reninangiotensin system in the DOCA-salt hypertensive rat (Basso et al. 1985 ;Igarashi et al. 1985;Itaya et al. 1986). Much less is known about the mechanisms mediating steroid hypertension in the dog ; however, it would seem that the sympathetic nervous system does not play a primary role in canine DOCA-or DOCA-salt hypertension (Bravo et al. 1977 ;Zeigler and Zimmerman 1987;Ueno

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Changes in renal vascular reactivity at various stages of deoxycorticosterone hypertension in rats.

Cited by 83 publications

References 24 publications

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Abnormal vascular phosphoinositide hydrolysis in the spontaneously hypertensive rat

Renal Hemodynamics in Canine DOCA-Salt Hypertension: Effect of Calcium Channel Blockade.

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