K
Kumud Srivastava
Researcher at University of Mississippi Medical Center
Publications - 6
Citations - 673
Kumud Srivastava is an academic researcher from University of Mississippi Medical Center. The author has contributed to research in topics: Mean arterial pressure & Blood pressure. The author has an hindex of 5, co-authored 6 publications receiving 647 citations.
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Journal ArticleDOI
Gender Differences in Development of Hypertension in Spontaneously Hypertensive Rats: Role of the Renin-Angiotensin System
TL;DR: The data suggest that the development of hypertension in SHR regardless of sex steroids is mediated by the renin-angiotensin system, however, the data further suggest that androgens promote the exacerbation of pulmonary arterial pressure in male SHR via a mechanism involving the ren in-angiotsin system.
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Gender Differences in Hypertension in Spontaneously Hypertensive Rats: Role of Androgens and Androgen Receptor
TL;DR: In this paper, the androgen receptor plays a role in hypertension in male SHR and whether testosterone alone can cause the hypertension or whether conversion to dihydrotestosterone is necessary.
Journal ArticleDOI
Potassium inhibits free radical formation.
TL;DR: Physiological increases in potassium concentration inhibit the rate of superoxide anion formation by cell lines derived from endothelium and from monocytes/macrophages and reactive oxygen species formation by human white blood cells.
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Subpressor Doses of Angiotensin II Increase Plasma F 2 -Isoprostanes in Rats
Jane F. Reckelhoff,Huimin Zhang,Kumud Srivastava,L. Jackson Roberts,Jason D. Morrow,J. Carlos Romero +5 more
TL;DR: These studies suggest that low doses of Ang II are capable of producing oxidative stress in animals, and whether oxidative stress plays a causative role in Ang II-mediated slow-response hypertension or is secondary to the hypertension is not clear.
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Instability of Frog Virus 3 mRNA in Productively Infected Cells
TL;DR: Results indicate that viral transcripts were not preferentially stabilized in FV3-infected cells and suggest that the high steady-state level of viral messages present at late times after infection was due to viral transcription outpacing message degradation.