[Acute hemodynamic and hormonal effects of enalapril in essential hypertension: relations between hormone levels and efficacy].
0
Citation
0
Reference
10
Related Paper
Keywords:
Essential hypertension
Cite
We have shown previously that continuous (6 days) intracerebroventricular (ICV) leptin infusion in normal rats resulted in decreases in food intake and body weight. A reduction of food intake imposed on control rats (pair-feeding), aimed at mimicking leptin-induced hyperphagia, produced a marked decrease in the expression of muscle uncoupling protein-3 (UCP-3), whereas ICV infusion of leptin prevented such a decrease in UCP-3. To investigate an involvement of thyroid hormones in this effect of leptin, plasma levels of these hormones were determined in ICV leptin-infused, ICV vehicle-infused ad libitum fed or pair-fed controls. ICV leptin infusion and pair-feeding resulted in decreased plasma thyroid-stimulating hormone (TSH) and T4 levels relative to ad libitum fed controls. ICV leptin infusion maintained plasma levels of T3, but the levels were decreased by pair-feeding. The activity of the enzyme (hepatic 5'-monodeiodinase) responsible for T4/T3 conversion was measured. In the leptin-infused group, the activity of 5'-monodeiodinase was maintained at the values measured in ad libitum fed rats; in pair-fed rats, activity was reduced. Thus, conversion of T4 to T3 is decreased by pair-feeding, whereas such is not the case during leptin infusion. To further substantiate an involvement of thyroid hormones in the effect of leptin on muscle UCP-3 expression, hypothyroid rats were ICV infused with leptin or vehicle. It was observed that in hypothyroid rats, ICV leptin was unable to maintain muscle UCP-3 expression at values measured in ad libitum fed controls. These results suggest that central leptin stimulates T3 production via an activation of T4 to T3 conversion, and that this stimulation could be responsible for the effect of leptin on muscle UCP-3 expression. Thyroid hormones could thus be important mediators of the effect of leptin on energy expenditure.
Cite
Citations (52)
ABSTRACT The possible role of thyroid hormones in the rise in plasma GH observed in protein-restricted chicks was examined. Increased sensitivity of protein-restricted chicks to secretagogue challenge (TRH or GH-releasing factor) appears to account, at least in part, for increased GH concentrations in protein-restricted chicks. Thyroid hormones administered acutely were able to suppress plasma GH concentrations in protein-restricted chicks. Further, chronic thyroid hormone supplementation to low protein diets normalized circulating thyroid hormone concentrations and also normalized the response to GH secretagogue challenge. This decreased sensitivity to TRH provocation occurred without an accompanying change in plasma concentrations of insulin-like growth factor-I, a reputed inhibitor of GH secretion in the chicken. J. Endocr. (1988) 117, 223–228
Secretagogue
Fowl
Cite
Citations (15)
Observations on the effect of thyroid hormones on mouse submaxillary gland epidermal growth factor (EGF) and on the complementary effect of EGF on cultured thyroid cells led us to examine the interaction between EGF and thyroid hormones in the whole animal, during and after 24 h of infusion of 3.3 μg/kg-h mouse EGF into 6 merino ewes. There was a profound depression of both circulating T4 and T3 levels, to less than 20% of saline-infused control values, extending beyond the end of infusion. Plasma TSH concentrations were unchanged during the first 8 h of the infusion, excluding the likelihood of a suppressive effect of EGF on the hypothalamic-pituitary axis. Serum rT3 and 3,3′-diiodothyronine, however, experienced a more transitory 6-fold increase. These findings are consistent with a dual inhibitory effect of EGF on both thyroid hormone secretion and peripheral metabolism. (Endocrinology119: 214–217,1986)
Cite
Citations (30)
Growth hormone (GH) and the thyroid hormones interact in the hypothalamus, pituitary and peripheral tissues. Thyroid hormone exerts a permissive effect upon the anabolic and metabolic effects of GH, and increases pituitary synthesis of this protein hormone. GH depresses the secretion of thyrotropin and the thyroid hormones and increases the peripheral conversion of thyroxine to triiodothyronine. In the adult male rat experimental hypothyroidism produced by ingestion of propylthiouracil depresses the GH secretory response to GH-releasing hormone in vivo and in vitro, reflecting the lowered pituitary stores of GH in the hypothyroid state. Short term administration of large amounts of thyroxine with induction of the hyperthyroid state does not affect the in vivo GH secretory response to GH-releasing hormone in this animal.
Propylthiouracil
Endocrine gland
Cite
Citations (25)
Rats were thyroidectomized (T) and injected once daily with thyroxine (T4) or triiodothyronine (T3) ip; circulating thyrotropin (TSH) levels and TSH response to 100 ng of thyrotropin releasing hormone (TRH) iv, were measured in different groups of rats at several intervals after the last dose of T4 or T3. It was found that T rats on 1.8 mug T4 or 0.4 mug T3/100 g BW/day, response to TRH decreased after the injection of the hormone, maximum suppressive effect being found about 7-8 h after T4, or 4 h after T3. The response increased as T4 or T3 levels reached a nadir, in agreement with present views on TRH, T4, and T3 interactions at the pituitary level. The degree of TSH response to TRH appears as a sensitive parameter of T4 or T3 activity in this experimental model. However, in T rats on 0.2 mug T3/100 g BW/day, TSH response to TRH did not decrease, but actually increased, after the daily injection of T3. These animals appeared to be in a state of continuous thyroid hormone deficiency. The same 0.2 mug T3 dose effectively suppresses the elevated basal TSH levels of these animals. It is also capable of decreasing TSH response to 100 ng TRH in animals under more "euthyroid" conditions. These results in the T rats on 0.2 mug T3 are not easily fitted into the relatively simple model frequently described to explain TRH-T3 interactions and TSH secretion.
Basal (medicine)
TRH stimulation test
Cite
Citations (41)
Spontaneously hypertensive rat
Cite
Citations (29)
Sodium restriction enhances the aldosterone response to angiotensin-II (All) in normal rats, but not in spontaneously hypertensive rats (SHR). To determine whether a change and/or abnormality in the circulating or adrenal reninangiotensin systems are responsible for these observations, three groups of animals were studied on a low sodium diet with and without the administration of a converting enzyme inhibitor (enalapril). Sprague-Dawley and Wistar-Kyoto (normotensive rat strains) and SHR were placed on low sodium (0.1%) for 9 days, the last 4 days of which enalapril was administered to half of the animals. In all groups enalapril treatment resulted in a significant (P < 0.001) reduction in blood pressure, an increase in renin activity, and a reduction in plasma aldosterone when all of the animals were considered together, although the change in blood pressure achieved statistical significance only in the Wistar-Kyoto rats. Additionally, basal aldosterone output from isolated glomerulosa cells was lower in the normotensive animals pretreated with enalapril. However, despite the evidence for inhibition of converting enzyme, there was no change in the hypertensive animals. Thus, neither locally nor systemically generated All appear to participate in the maintenance of the increased aldosterone responsiveness to All with sodium restriction. Furthermore, they do not appear to contribute to the altered adrenal responsiveness to All with sodium restriction in SHR. These data provide further support for the hypothesis that as yet undefined glomerulosa intracellular mechanisms are altered by dietary sodium restriction in normotensive, but not hypertensive, rats.
Low sodium diet
Mineralocorticoid
Plasma renin activity
Cite
Citations (7)
Adult male Sprague-Dawley rats were made diabetic with streptozotocin (40 mg/kg BW). The effect of treatment with insulin, LH, or both hormones during the experimental period on serum levels of testosterone (T) and dihydrotestosterone (DHT), as well as testicular Δ 5-3β-hydroxysteroid dehydrogenase (3β-HSD) activity was measured 15 days (intact rats) or 10 days (hypophysectomized rats) after the induction of diabetes. In intact rats, diabetes resulted in a marked reduction in serum hormone levels and testicular 3β-HSD activity. Insulin or LH treatment significantly increased hormone levels and testicular 3β-HSD activity in diabetic rats. The administration of both hormones to diabetic rats resulted in a rise in enzyme activity to values similar to those in the normoglycemic controls, with a concomitant increase in serum hormone levels. In hypophysectomized diabetic rats, insulin resulted in testicular 3β- HSD activity and serum hormone concentrations similar to those in normoglycemic hypophysectomized rats. Treatment with LH significantly increased 3β-HSD activity and the serum levels of T and DHT in hypophysectomized normoglycemic and hypophysectomized diabetic animals compared to those in the hypophysectomized untreated controls. When the results were expressed in terms of 3β-HSD activity per testis weight, it became evident that treatment of diabetic hypophysectomized rats with both hormones increased 3β-HSD activity to levels similar to those obtained in the normoglycemic hypophysectomized animals treated with LH alone. In both experiments, the stimulatory effects of insulin and LH on the serum levels of T and DHT followed a pattern similar to that the effects of insulin and LH on the activity of the testicular 3β-HSD. The results of this study serve as further evidence of testicular failure in diabetic rats and suggested that an inadequate steroidogenesis in the testes of diabetic rats may be due, at least in part, to decreased 3β-HSD ctivity. Based on the parameters studied, a synergistic action could be observed after daily treatment with insulin and LH. This fact supports previous findings of a stimulatory effect of insulin on LH receptors in the testis of the diabetic rat and suggests that in the testes, 3β-HSD is regulated by LH and insulin.
Dihydrotestosterone
Hypophysectomy
Cite
Citations (28)
Holstein heifers were treated with synthetic thyrotropin-releasing hormone (TRH) or saline twice daily from one week through 6 mo of age. Plasma concentrations of prolactin (PRL) and thyrotropin (TSH) were elevated (P<.01) within 30 min after the first TRH injection (1 week of age). At 1 and 3 mo of treatment, PRL and TSH increased in response to TRH, although the TSH response was reduced (P < .01) as compared to the first day of treatment. Although plasma growth hormone (GH) appeared to be elevated following the first TRH injection, this effect was not statistically significant (P>.05), nor was it significantly influenced by treatment following subsequent TRH injections. None of the 3 hormones, PRL, TSH or GH, was elevated following the final TRH injection at 6 mo of age. In contrast, plasma concentrations of PRL and TSH were increased in a control heifer injected with TRH at 6 mo. These data indicate that hormonal responsiveness to TRH stimulation decreases with continued twice daily treatment at doses of TRH used in the present studies. Examination of weight gains indicated that chronic treatment with TRH was associated with increased growth rate through 6 mo of age (10.6% increased average daily gains P<.10), which was exhibited in a steeper slope (P < .05) of the growth curve in the TRH group. Feed intake was slightly greater in TRH heifers, although feed efficiency (kg feed/ kg gain) was not different between the two groups. Plasma concentrations of PRL increased (P < .01) with age (r = †0.938) in control heifers while plasma TSH and GH were not significantly related to age. This observation establishes a positive correlative elationship between PRL secretion and the approach of puberty in the dairy heifer. It was also noted that elevation of PRL secretion by TRH treatment was associated with significant advancement of age at first observed estrus (9.4 vs.10.5 mo) suggesting that a functional relationship between PRL secretion and puberty may exist in dairy heifers. (Endocrinology100: 1394, 1977)
Cite
Citations (19)
Fasting in rodents is characterized by decreases in serum T4 and T3 levels but no compensatory increase in serum TSH level. The types 1 and 2 deiodinases (D1 and D2) are postulated to play key roles in mediating these changes. However, serum T4 and T3 levels in fasted 5′-deiodinase-deficient mice decreased by at least the same percentage as that observed in wild-type mice, whereas serum TSH level was unaffected. D3 activity was increased in kidney, muscle, and liver up to 4-fold during fasting, and the mean serum rT3 level was increased 3-fold in fasted D1-deficient mice, compared with fed animals. In wild-type mice, the tissue contents of T4 and T3 in liver, kidney, and muscle were unchanged or increased in fasted animals, and after the administration of [125I]T4 or [125I]T3, the radioactive content in the majority of tissues from fasted mice was increased 2- or 4-fold, respectively. These findings suggest that the observed fasting-induced reductions in the circulating T3 and T4 levels are mediated in part by increased D3 activity and by the sequestration of thyroid hormone and their metabolites in tissues. Studies performed in D3-deficient mice demonstrating a blunting of the fasting-induced decrease in serum T4 and T3 levels were consistent with this thesis. Thus, the systemic changes in thyroid hormone economy as a result of acute food deprivation are not dependent on the D1 or D2 but are mediated in part by sequestration of T4 and T3 in tissues and their enhanced metabolism by the D3.
DIO2
Cite
Citations (32)