Involvement of atrial natriuretic peptide in blood pressure reduction induced by estradiol in spontaneously hypertensive rats

Belo, Najara O.; Silva-Barra, Juliana; Cárnio, Evelin C.; Antunes‐Rodrigues, José; Gutkowska, Jolanta; Reis, Adelina Martha dos

doi:10.1016/j.regpep.2003.10.007

Cited by 26 publications

(30 citation statements)

References 40 publications

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“…In ovariectomized rats, estradiol treatment reduces blood pressure and increases the synthesis and release of ANP [10]. Indeed, in human studies, higher circulating levels of ANP have been observed in premenopausal women, compared with men [11], [12].…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in the Beneficial Cardiac Effects of Chronic Treatment with Atrial Natriuretic Peptide In Spontaneously Hypertensive Rats

Romero¹,

Caniffi²,

Bouchet³

et al. 2013

PLoS ONE

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IntroductionThe aim of this study was to investigate both the effects of chronic treatment with atrial natriuretic peptide (ANP) on systolic blood pressure (SBP), cardiac nitric oxide (NO) system, oxidative stress, hypertrophy, fibrosis and apoptosis in spontaneously hypertensive rats (SHR), and sex-related differences in the response to the treatment.Methods10 week-old male and female SHR were infused with ANP (100 ng/hr/rat) or saline (NaCl 0.9%) for 14 days (subcutaneous osmotic pumps). SBP was recorded and nitrites and nitrates excretion (NOx) were determined. After treatment, NO synthase (NOS) activity, eNOS expression, thiobarbituric acid-reactive substances (TBARS) and glutathione concentration were determined in left ventricle, as well as the activity of glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD). Morphological studies in left ventricle were performed in slices stained with hematoxylin-eosin or Sirius red to identify collagen as a fibrosis indicator; immunohistochemistry was employed for identification of transforming growth factor beta; and apoptosis was evaluated by Tunel assay.ResultsFemale SHR showed lower SBP, higher NO-system activity and less oxidative stress, fibrosis and hypertrophy in left ventricle, as well as higher cardiac NOS activity, eNOS protein content and NOx excretion than male SHR. Although ANP treatment lowered blood pressure and increased NOS activity and eNOS expression in both sexes, cardiac NOS response to ANP was more marked in females. In left ventricle, ANP reduced TBARS and increased glutathione concentration and activity of CAT and SOD enzymes in both sexes, as well as GPx activity in males. ANP decreased fibrosis and apoptosis in hearts from male and female SHR but females showed less end-organ damage in heart. Chronic ANP treatment would ameliorate hypertension and end-organ damage in heart by reducing oxidative stress, increasing NO-system activity, and diminishing fibrosis and hypertrophy.

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Section: Introductionmentioning

confidence: 99%

Sex Differences in the Beneficial Cardiac Effects of Chronic Treatment with Atrial Natriuretic Peptide In Spontaneously Hypertensive Rats

Romero¹,

Caniffi²,

Bouchet³

et al. 2013

PLoS ONE

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“…OVX rats received daily injections of E 2 (E 2 group: 5 µg·100 g −1 ·day −1 , SARSA, Hoechst Marion Roussel, France; young, N = 11, middle-aged, N = 7) or vehicle (vehicle group: 0.1 mL corn oil·100 g −1 ·day −1 ; young, N = 7, middle-aged, N = 10) for 4 days. We chose the dose and duration of treatment with E 2 (4 days) based on a previous study by Belo et al (12). In the cited study, the authors showed that short-term E 2 treatment (5 µg·100 g −1 ·day −1 for 4 days) reduced the arterial pressure of ovariectomized animals.…”

Section: Methodsmentioning

confidence: 99%

“…In spite of this, short-term estrogen therapy might be an important strategy to treat cardiovascular diseases. Indeed, short-term administration of E 2 to ovariectomized spontaneously hypertensive rats (SHR) causes a significant reduction in blood pressure on the fourth day of treatment (12), suggesting that the beneficial effects of E 2 on the cardiovascular system can be already observed after a few days of hormonal supplement. Thus, the aim of the present study was to investigate the effects of short-term estrogen administration on cardiac reperfusion arrhythmias in young and middle-aged rats since age-related differences might change the cardiovascular responses to the administration of E 2 .…”

Section: Introductionmentioning

confidence: 99%

Effects of short-term administration of estradiol on reperfusion arrhythmias in rats of different ages

Savergnini

Reis

Santos

et al. 2012

Braz J Med Biol Res

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Little is known about age-related differences in short-term effects of estradiol on ischemia-reperfusion (I/R) insults. The present study was designed to evaluate the effects of short-term treatment with estradiol on reperfusion arrhythmias in isolated hearts of 6-7-week-old and 12-14-month-old female rats. Wistar rats were sham-operated, ovariectomized and treated with vehicle or ovariectomized and treated with 17β-estradiol (E2; 5 µg·100 g−1·day−1) for 4 days. Hearts were perfused by the Langendorff technique. Reperfusion arrhythmias, i.e., ventricular tachycardia and/or ventricular fibrillation, were induced by 15 min of left coronary artery ligation and 30 min of reperfusion. The duration and incidence of I/R arrhythmias were significantly higher in young rats compared to middle-aged rats (arrhythmia severity index: 9.4 ± 1.0 vs 3.0 ± 0.3 arbitrary units, respectively, P < 0.05). In addition, middle-aged rats showed lower heart rate, systolic tension and coronary flow. Four-day E2 treatment caused an increase in uterine weight. Although E2 administration had no significant effect on the duration of I/R arrhythmias in middle-aged rats, it induced a marked reduction in the rhythm disturbances of young rats accompanied by a decrease in heart rate of isolated hearts. Also, this reduction was associated with an increase in QT interval. No significant changes were observed in the QT interval of middle-aged E2-treated rats. These data demonstrate that short-term estradiol treatment protects against I/R arrhythmias in hearts of young female rats. The anti-arrhythmogenic effect of estradiol might be related to a lengthening of the QT interval.

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“…The central mechanisms implicated in mineralocorticoid effects comprise the increase of sympathetic outflow and inflammatory cytokines (44), interactions with the vasoactive neuropeptides angiotensin II (AngII), natriuretic peptides, and arginine vasopressin (11,45,46) and deleterious remodeling of the cerebral vasculature with exacerbation of ischemic damage (15). Two proteins induced by mineralocorticoids in the kidney, the Na,K-ATPase and the sodium channel, are also upregulated by mineralocorticoids in the brain (43,47).…”

Section: Figurementioning

confidence: 99%

“…The involvement of mineralocorticoids and MR is more obvious in the hypertension of DOCAqsalt-treated rats. DOCA-derived deoxycorticosterone can occupy and activate brain MR, eliciting typical mineralocorticoid-responses including induction of salt appetite, increased AVP synthesis, increased angiotensin II binding and development of hypertension (22,45,65). Furthermore, i.c.v.…”

Section: Neurotoxic and Neuroprotective Effects Of Steroids In The Brmentioning

confidence: 99%

Protective effect of estrogens on the brain of rats with essential and endocrine hypertension

Nicola¹,

Pietranera²,

Bellini

et al. 2010

Hormone Molecular Biology and Clinical Investigation

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Estrogen neuroprotection has been shown in pathological conditions damaging the hippocampus, such as trauma, aging, neurodegeneration, excitotoxicity, oxidative stress, hypoglycemia, amyloid-β peptide exposure and ischemia. Hypertensive encephalopathy also targets the hippocampus; therefore, hypertension seems an appropriate circumstance to evaluate steroid neuroprotection. Two experimental models of hypertension, spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)-salt hypertensive rats, develop hippocampal abnormalities, which include decreased neurogenesis in the dentate gyrus, astrogliosis, low expression of brain-derived neurotrophic factor (BDNF) and decreased number of neurons in the hilar region, with respect of their normotensive strains Wistar Kyoto (WKY) and Sprague-Dawley rats. After estradiol was given for 2 weeks to SHR and DOCA-treated rats, both hypertensive models normalized their faulty hippocampal parameters. Thus, estradiol treatment positively modulated neurogenesis in the dentate gyrus of the hippocampus, according to bromodeoxyuridine incorporation and doublecortin immunocytochemistry, decreased reactive astrogliosis, increased BDNF mRNA and protein expression in the dentate gyrus and increased neuronal number in the hilar region of the dentate gyrus. A role of local estrogen biosynthesis is suggested in SHR, because basal aromatase mRNA in the hippocampus and immunoreactive aromatase protein in cell processes of the dentate gyrus were highly expressed in these rats. Estradiol further stimulated aromatase-related parameters in SHR but not in WKY. These observations strongly support that a combination of exogenous estrogens to those locally synthesized might better alleviate hypertensive encephalopathy. These studies broaden estrogen neuroprotective functions to the hippocampus of hypertensive rat models.

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Involvement of atrial natriuretic peptide in blood pressure reduction induced by estradiol in spontaneously hypertensive rats

Cited by 26 publications

References 40 publications

Sex Differences in the Beneficial Cardiac Effects of Chronic Treatment with Atrial Natriuretic Peptide In Spontaneously Hypertensive Rats

Sex Differences in the Beneficial Cardiac Effects of Chronic Treatment with Atrial Natriuretic Peptide In Spontaneously Hypertensive Rats

Effects of short-term administration of estradiol on reperfusion arrhythmias in rats of different ages

Protective effect of estrogens on the brain of rats with essential and endocrine hypertension

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