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Reducing endogenous estrogen leads to increased proliferation of porcine Sertoli cells during the first 2 months of life. The resulting increase in porcine Sertoli cell numbers is maintained through puberty. The reduced estrogen appears to be the direct hormonal mediator because essentially no changes are observed in other hormones. However, the mechanism for this effect on Sertoli cell proliferation is unknown. The objective of these studies was to evaluate estrogen receptors alpha and beta (ESR1 and ESR2) in conjunction with androgen receptor (AR) on Sertoli cells and other testicular cell types, as an initial step toward understanding how reduced estrogen leads to increased Sertoli cell numbers. Testis sections from treated animals (aromatase inhibition to decrease endogenous estrogen beginning at 1 week of age) and from littermate controls treated with vehicle were subjected to immunocytochemical labeling for ESR1, ESR2, and AR. Three observers scored Sertoli cells, interstitial cells, peritubular myoid cells, and germ cells for intensity of labeling (0: absent; 1+: weak; 2+: moderate; or 3+: strong labeling). AR in Sertoli cells was readily detected at 1 week of age, was very faint in 2-month vehicle controls, and labeling appeared to increase in 3-month vehicle controls. AR in Sertoli cells, interstitial cells, and apparently germ cells was increased in treated animals at 2 months of age compared with the vehicle controls. This increase was confirmed in western blots. ESR1 and ESR 2 were clearly present in Sertoli cells from 1-week-old animals; ESR in Sertoli cells generally decreased with age with the decrease more apparent for ESR2. ESR1 in Sertoli cells and peritubular myoid cells exhibited some treatment-related effects but reduction of endogenous estrogen did not appear to affect ESR2 in the boar testis. The observed alterations in AR and ESR1 may mediate the increases in Sertoli cell proliferation following inhibition of endogenous estrogen production or may reflect the altered function of the Sertoli cells and peritubular myoid cells.

Background: Hypertension is one of the most prevalent noncommunicable diseases. The Joint National Commission VIII guidelines recommend angiotensin receptor blockers (ARBs) as the first‑line drug and addition of hydrochlorothiazide (HCTZ) increases their efficacy. Olmesartan medoxomil is recently introduced, whereas telmisartan is a relatively older ARB. This study was conducted to assess the efficacy and safety of olmesartan and HCTZ versus telmisartan and HCTZ in the treatment of mild‑to‑moderate hypertension. Materials and Methods: A total of 120 patients with mild‑to‑moderate hypertension were recruited and randomized to receive either olmesartan 20 mg+HCTZ 12.5 mg (Group O) or telmisartan 40 mg+HCTZ 12.5 mg (Group T) orally once daily for 8 weeks. Blood pressure (BP) and heart rate were recorded at baseline and at 4th and 8th weeks, but blood sugar and lipid profile were estimated at baseline and 8th week. Results: Forty‑six Group O and 44 Group T patients completed the study. Majority of patients were in the fifth decade of life (72.3%), 56% were males, and 35% had type II diabetes mellitus and received oral antidiabetics. The mean BP was 148.6 ± 5.9/89.2 ± 5.9 and 147.9 ± 5.2/88.1 ± 4.2 mmHg at baseline and decreased significantly at week 8 (131.0 ± 5.4/80.3 ± 2.9 and 136.8 ± 5.5/83.6 ± 3.9 mmHg) in Group O and Group T respectively. Patients in Group O had significant reduction in systolic BP (SBP) (P = 0.0001) and diastolic BP (P = 0.04) than that in Group T. More than 10 mmHg decrease in SBP was observed in 86.9% versus 65.9% of patients in Group O and Group T, respectively, which was statistically significant (P = 0.01). Diabetic patients in both groups had a significant decrease in blood sugar by week 8, but intergroup comparison was insignificant. Change in heart rate and lipid profile was negligible. Common adverse effects were dizziness, abdominal pain and pedal edema in both groups. Conclusion: Olmesartan + HCTZ was more effective than telmisartan + HCTZ in lowering BP.