Supaporn Kulthinee

The sympathetic nervous responses to cold stress are known; however, concurrent cardiovascular and ocular parameter alterations in the responses are poorly characterized. The aim of this study was to examine the influence of the cold pressor test (CPT) on cardiovascular and ocular parameters in young adult subjects. There was a total of 86 participants. The CPT was conducted by submerging each participant’s left hand in cold water (3–5 °C) for 3 min. During the CPT, systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), and heart rate were found to be significantly increased compared to the baseline and significantly decreased compared to recovery, including the mean of the standard deviations of all normal-to-normal intervals (SDNN). In the recovery phase, the SDNN continued to decrease statistically significantly compared to the baseline and the CPT. Furthermore, the findings of this study show that the CPT impacted intra-ocular pressure (IOP), ACD, and pupil size parameters. There was a positive correlation between the MAP and IOP in both eyes during the CPT. The cold stress stimulates a sympathetic response, leading to an increase in the MAP. The pupil size increased in response to the CPT in both eyes, indicating that ocular function was increased in response to the CPT in young adults compared to baseline. In conclusion, our results suggest that in young adults, cardiovascular and ocular parameters respond to the sympathetic nervous system during the CPT.

Glomerular arteriolar vasoconstriction and tubulointerstitial injury are observed before glomerular damage occurs in models of hypertension. High interstitial ATP concentrations, caused by the increase in arterial pressure, alter renal mechanisms involved in the long-term control of blood pressure, autoregulation of glomerular filtration rate and blood flow, tubuloglomerular feedback (TGF) responses, and sodium excretion. Elevated ATP concentrations and augmented expression of P2X receptors have been demonstrated under a genetic background or induction of hypertension with vasoconstrictor peptides. In addition to the alterations of the microcirculation in the hypertensive kidney, the vascular actions of elevated intrarenal angiotensin II levels may be mitigated by the administration of broad purinergic P2 antagonists or specific P2Y12, P2X1, and P2X7 receptor antagonists. Furthermore, the prevention of tubulointerstitial infiltration with immunosuppressor compounds reduces the development of salt-sensitive hypertension, indicating that tubulointerstitial inflammation is essential for the development and maintenance of hypertension. Inflammatory cells also express abundant purinergic receptors, and their activation by ATP induces cytokine and growth factor release that in turn contributes to augment tubulointerstitial inflammation. Collectively, the evidence suggests a pathophysiological activation of purinergic P2 receptors in angiotensin-dependent hypertension. Coexistent increases in intrarenal angiotensin II and activates Ang II AT1 receptors, which interacts with over-activated purinergic receptors in a complex manner, suggesting convergence of their post-receptor signaling processes.