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Sodium-glucose cotransporter 2 inhibition does not improve the acute pressure natriuresis response in rats with type

Natalie K Jones1, Hannah M Costello1, Marie-Louise T Monaghan1

  • 1British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.

Experimental Physiology
|January 16, 2023
PubMed

Insights

Sodium-glucose cotransporter 2 (SGLT2) inhibitors do not improve renal pressure natriuresis in rats with or without type 1 diabetes mellitus. This suggests SGLT2 inhibitors

Area of Science:

  • Nephrology
  • Endocrinology
  • Cardiovascular Medicine

Background:

  • Type 1 diabetes mellitus (T1DM) is associated with increased cardiovascular and kidney disease risk, partly due to hypertension.
  • Impaired renal pressure natriuresis (PN), a mechanism regulating blood pressure, is a contributing factor in T1DM-related complications.
  • Sodium-glucose cotransporter 2 (SGLT2) inhibitors are known to reduce cardiovascular risk in patients with kidney disease.

Purpose of the Study:

  • To investigate whether SGLT2 inhibition can improve the renal pressure natriuresis (PN) response in the context of type 1 diabetes mellitus (T1DM).
  • To determine if SGLT2 inhibition enhances the body's ability to excrete sodium in response to increased blood pressure, a key factor in long-term blood pressure control.

Main Methods:

  • Adult male Sprague-Dawley rats, both non-diabetic and T1DM-induced, were used in the study.
  • Rats were administered dapagliflozin, an SGLT2 inhibitor, or a vehicle control under anesthesia.
  • Blood pressure was incrementally increased, and the resulting changes in sodium excretion (PN response) and urine output were measured.

Main Results:

  • Dapagliflozin did not enhance the acute in vivo pressure natriuresis response in either healthy or T1DM rats.
  • While dapagliflozin induced glycosuria, this effect was independent of blood pressure changes.
  • The impaired PN response observed in T1DM rats was not improved by dapagliflozin treatment.

Conclusions:

  • Inhibition of SGLT2 does not augment the pressure natriuresis response in rats, irrespective of their diabetic status.
  • SGLT2 plays a minimal role in tubular sodium reabsorption and does not appear to be the cause of impaired PN in T1DM.
  • The cardiovascular benefits of SGLT2 inhibitors are unlikely to be mediated through an enhanced natriuretic response to increased blood pressure.
Keywords:
SLGT2blood pressurediabetespressure natriuresissodium balance

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