- Secondary Hypertension
- Fluid and Electrolyte Disorders
Honors & Awards
Postdoctoral Fellowship, American Heart Association (1/1/2016-1/1/2018)
Tashia and John Morgridge Endowed Postdoctoral Fellow, Child Health Research Institute (7/1/2013-12/31/2015)
Medical Education:University of California San Diego Medical School (2008) CA
Board Certification: Nephrology, American Board of Internal Medicine (2015)
Fellowship:Stanford Hospital and ClinicsCA
Board Certification: Internal Medicine, American Board of Internal Medicine (2012)
Residency:Scripps Mercy Hospital (2012) CA
Internship:Scripps Mercy Hospital (2009) CA
Current Research and Scholarly Interests
Diabetes and hypertension are among the most common diseases treated in the US. The combination of these disease greatly increased the risk of heart attack, stroke, and early death. While over 90% of patients with diabetes have high blood pressure, its cause is unknown. Working in the laboratory of Vivek Bhalla, I am interested in understanding the mechanisms that diabetes contributes to high blood pressure. We current are focused on the regulatory role of insulin on sodium reabsorption in the kidney, which is a master regulator of blood pressure. Using a mouse model of diabetes and transgenic technologies, we utliize classical metabolic experiments, expression, electrophysiological, and primary cell culture techniques to understand the role of insulin in regulating sodium transport in the kidney, blood volume in the body, and increased blood pressure in diabetes.
Graduate and Fellowship Programs
Nephrology (Fellowship Program)
- Insights from direct renal insulin infusion: a new hammer for an age-old nail. American journal of physiology. Renal physiology 2017: ajprenal.00532.2017
Molecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome.
Current hypertension reports
2017; 19 (8): 60
We review the known mechanisms of sodium-sensitive hypertension in the metabolic syndrome with a focus on preclinical models, differences between these models, and methodological limitations. We also identify future directions for a better understanding and treatment of this common condition.Rigorous methodologies to measure blood pressure in preclinical models may clarify some of the inconsistencies in the literature. Renal, neural, hormonal, and cardiovascular systems are dysregulated and contribute to elevated blood pressure. Local renin-angiotensin systems enhance systemic hormone signaling to increase blood pressure. Since the original description of metabolic syndrome, investigators from many fields have contributed to an increasingly complex and mechanistic understanding of this common condition. These systems integrate to regulate sodium transport in the kidney leading to hypertension and enhanced sodium sensitivity. An array of non-uniform preclinical models are used and support clinical studies to inform which models are pathophysiologically relevant for further mechanistic studies to guide targeted therapy.
View details for DOI 10.1007/s11906-017-0759-5
View details for PubMedID 28676941
Na+-sensitive elevation in blood pressure is ENaC independent in diet-induced obesity and insulin resistance
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
2016; 310 (9): F812-F820
The majority of patients with obesity, insulin resistance, and metabolic syndrome have hypertension, but the mechanisms of hypertension are poorly understood. In these patients, impaired sodium excretion is critical for the genesis of Na(+)-sensitive hypertension, and prior studies have proposed a role for the epithelial Na(+) channel (ENaC) in this syndrome. We characterized high fat-fed mice as a model in which to study the contribution of ENaC-mediated Na(+) reabsorption in obesity and insulin resistance. High fat-fed mice demonstrated impaired Na(+) excretion and elevated blood pressure, which was significantly higher on a high-Na(+) diet compared with low fat-fed control mice. However, high fat-fed mice had no increase in ENaC activity as measured by Na(+) transport across microperfused cortical collecting ducts, electrolyte excretion, or blood pressure. In addition, we found no difference in endogenous urinary aldosterone excretion between groups on a normal or high-Na(+) diet. High fat-fed mice provide a model of metabolic syndrome, recapitulating obesity, insulin resistance, impaired natriuresis, and a Na(+)-sensitive elevation in blood pressure. Surprisingly, in contrast to previous studies, our data demonstrate that high fat feeding of mice impairs natriuresis and produces elevated blood pressure that is independent of ENaC activity and likely caused by increased Na(+) reabsorption upstream of the aldosterone-sensitive distal nephron.
View details for DOI 10.1152/ajprenal.00265.2015
View details for Web of Science ID 000375115700003
View details for PubMedID 26841823
Harvest and primary culture of the murine aldosterone-sensitive distal nephron.
American journal of physiology. Renal physiology
2015; 308 (11): F1306-15
The aldosterone-sensitive distal nephron (ASDN) exhibits axial heterogeneity in structure and function from the distal convoluted tubule to the medullary collecting duct. Ion and water transport is primarily divided between the cortex and medulla of the ASDN, respectively. Transcellular transport in this segment is highly regulated in health and disease and is integrated across different cell types. We currently lack an inexpensive, high-yield, and tractable technique to harvest and culture cells for the study of gene expression and physiologic properties of mouse cortical ASDN. To address this need, we harvested tubules bound to Dolichos biflorus agglutinin (DBA) lectin-coated magnetic beads from kidney cortex and characterized these cell preparations. We determined that these cells are enriched for markers of distal convoluted tubule, connecting tubule, and cortical collecting duct, including principal and intercalated cells. In primary culture these cells develop polarized monolayers with high-resistance (1000-1500 Ω*cm(2)), and maintain expression and activity of key channels. These cells demonstrate an amiloride-sensitive short-circuit current that can be enhanced with aldosterone and maintain measurable potassium and anion secretion. Our method can be easily adopted to study the biology of the ASDN and to investigate phenotypic differences between wild-type and transgenic mouse models.
View details for DOI 10.1152/ajprenal.00668.2014
View details for PubMedID 25810438
- Harvest and primary culture of the murine aldosterone-sensitive distal nephron. American journal of physiology. Renal physiology 2015; 308 (11): F1306-15