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Primary hyperaldosteronism
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Vivek Alaigh, Amanda Fernandes
There are several factors that stimulate renin release. The ovaries have been shown to produce prorenin, the precursor protein for renin, which may have a downstream effect on the RAAS.6 Prorenin levels peak around week 6–8 of gestation.7 In addition to the ovaries, the placenta also stimulates renin production. It has been estimated that the combination of the extra-renal and renal sources of renin cause the plasma renin activity (PRA) to increase almost 7-fold by the third trimester.4 Renin levels then drop following delivery.8
The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
Cryoactivation of human plasma renin55 has been reported to occur maximally at -5°C and pH 7.0.71 Under these conditions, inactive renin was found at two to three times the concentration of active renin in plasma.72 In anephric patients, the level of plasma “prorenin” averaged 61% of normal, while active renin was only 7% of normal.72,73 Although these workers called this material “prorenin,” the evidence that it is related to renin is at present incomplete. It depends on the similar pH optima of cryoactivated “prorenin’’ and active renin and on indirect evidence that the in vitro activity of both enzymes may be dependent on plasma-renin substrate concentration.
The development of hypertension in transgenic rats, TGR (mREN2)27
Published in H. Saito, Y. Yamori, M. Minami, S.H. Parvez, New Advances in SHR Research –, 2020
Jörg Peters, Detlev Ganten, John J. Mullins
The major function of the renin-angiotensin system is the regulation of blood pressure, water and electrolyte balance. Its effector peptide, angiotensin II (ANG II), is a strong vasopressor, which in addition stimulates the synthesis of several adrenal steroids particularly that of aldosterone, in the zona glomerulosa. ANG II also leads to sodium and water reabsorbtion in the kidney, has positive inotropic actions in the heart, is known to regulate blood pressure by direct actions in the brain, and is part of an important feedback-loop in the regulation of renal renin secretion. Furthermore, a role for angiotensins in the genesis of cardiac and arterial hypertrophy has been hypothesized and Sealey and colleagues (Sealey et al., 1985, 1986) have proposed additional roles for prorenin apart from simply being the precursor of active renin. Functional roles for circulating prorenin or extrarenal derived renin, however, have yet to be clearly defined.
Ovarian steroid cell tumor (not otherwise specified) with subsequent spontaneous pregnancy after tumor removal: a case report and literature review
Published in Gynecological Endocrinology, 2023
Phawat Matemanosak, Krantarat Peeyananjarassri, Chitkasaem Suwanrath, Saranya Wattanakumtornkul, Satit Klangsin, Ekasak Thiangphak, Kanet Kanjanapradit
The patient was diagnosed with a steroid cell tumor NOS of the ovary. These tumors can occur between the ages of 3 and 93 years, with an average age of 43 years. Most tumors are unilateral, with only 6% of patients being found to be bilateral. Three-fourths of steroid cell tumor NOS can secrete a variety of hormones, including testosterone, estradiol, cortisol, and infrequently prorenin [1]. Most of these tumors secrete testosterone, which causes hirsutism or virilization accounting for 56–77% of cases [1,7]. Approximately 6–23% secrete estrogen, which is associated with abnormal uterine bleeding or postmenopausal bleeding [1,7]. In addition, endometrial adenocarcinoma has been reported in women with ovarian tumors [8], and 6–10% of cases are associated with Cushing’s syndrome [9,10]. Rarely, hypertension and hypokalemia can also be unique presentations in cases of elevated serum prorenin levels from ovarian steroid cell tumors [11].
Type 2 diabetes mellitus and cardiovascular risk; what the pharmacotherapy can change through the epigenetics
Published in Postgraduate Medicine, 2020
Pavlina A. Andreeva–Gateva, Ivelina D. Mihaleva, Ivanka I. Dimova
The renin-angiotensin system (RAS) is a cascade of successive activation of proteases starting from the renin with one of the important final effects on the aldosterone secretion, i.e. renin-angiotensin-aldosterone system (RAAS). Renin is produced from the juxtaglomerular apparatus as an inactive prorenin and sympathetic system by beta1-receptors, prostaglandins, and kinins can stimulate renin secretion. According to the classical, endocrine view of the systemic RAS, renin catalyzes the cleavage of angiotensin I, from the circulating angiotensinogen, a protein produced by the liver. Angiotensin I is subsequently hydrolyzed by angiotensin I-converting enzyme (ACE), located on endothelial cells, yielding the angiotensin II, the active end product of the RAS cascade [98]. Epigenetic mechanisms are involved in the regulation of the renin secretion by histone H4 acetylation [99]. Epigenetic regulation of the ACE expression via hypermethylation of the promoter region by the inflammatory cytokine TNFα in the endothelial cells was recently reported [100].
Aliskiren and valsartan in combination is a promising therapy for hypertensive renal injury in rats
Published in Clinical and Experimental Hypertension, 2018
In addition, aliskiren could neutralize the (P)RR-mediated activation of prorenin and the consequent gain in Ang II forming ability. As aliskiren once bound to “open” prorenin, it is unlikely to dissociate, because of its high affinity for the active site. Moreover, this binding should block any enzymatic activity gained by (non)-proteolytic activation of the molecule. Consequently, the tissue damage related to angiotensin generated by (P)RR-bound, nonproteolytically activated prorenin, or prorenin that becomes proteolytically activated at tissue sites should be reduced by aliskiren Feldman et al. (6). The above authors explained that the renoprotective effect of aliskiren was attributed to its extensive partitioning to the kidney, achieving a kidney/plasma concentration ratio of over 60 at 2 weeks of treatment. In addition, Huang et al. (21) showed that in cultured mesangial cells, stimulation of the (P)RR with renin resulted in TGF-β1 (transforming growth factor β1) production and extracellular matrix protein synthesis, and that suppressing the (P)RR inhibited the production of these latter factors.