Graduate Student Western University of Health Sciences Pomona, California, United States
Angela Reinert (Western University of Health Sciences)| Simon Bulley (Western University of Health Sciences)
In the body, the state of dehydration occurs where there is a deficit of water compared to that which is required to function properly. Water transportation is crucial and carried out via aquaporins (AQPs) located throughout the body and as a response to dehydration events, hormones such as angiotensin II (Ang II) and arginine-vasopressin (AVP) are secreted to induce various normal physiological functions via a hormone-specific receptor and associated-receptor activation found in vascular smooth muscle cells (VSMCs). Consequently, dehydration results with overall blood vessel constriction and thickening of the blood, ultimately leading to heart strain and increased blood pressure. Currently, the effect of dehydration on both the angiotensin II receptor type 1 (AT1R) and vasopressin receptor (V1R) expressed in resistance-sized artery VSMCs is unclear. C57BL/6J male mice were deprived of water for 48 hours before analyzing AT1R and V1R expression and function in freshly isolated mesenteric arteries, compared to controls. Dehydration for 48 hours results in a reduction in AT1R and V1R message and protein expression as well as a reduction in angiotensin- and arginine vasopressin (AVP)-induced vasoconstriction in pressurized mesenteric arteries. These data suggest that AT1R and V1R function is reduced in resistance-sized mesenteric arteries as a response to an elevation in plasma vasopressin and angiotensin II that occurs after dehydration.