BP Medications at Night Reduces Diabetes Risk
By HospiMedica International staff writers Posted on 05 Oct 2015 |
Taking hypertension medication before sleep, rather than in the morning, not only lowers nighttime blood pressure (BP) but protects against new-onset diabetes, according to a new study.
Researchers at the University of Vigo (Spain) conducted a prospective study involving 2,012 hypertensive patients (976 men, 1,036 women, and average age 53) without diabetes, who were randomized via a computer-generated allocation table to ingest their prescribed hypertension medications upon awakening or at bedtime. Investigators blinded to the hypertension treatment scheme of the patients then assessed the development of new-onset diabetes. Participants were followed for a mean 5.9 years.
The results showed that 171 participants developed type 2 diabetes during follow-up. Patients of the bedtime ingestion group showed significantly lower asleep BP and significantly lower risk of new-onset diabetes, after adjustment for fasting glucose, waist circumference, asleep systolic mean BP, dipping classification, and chronic kidney disease (CKD). The researchers observed greater benefit with medications that block the renin-angiotensin-aldosterone system (RAAS), such as angiotensin receptor blockers (ARBs), ACE inhibitors, and β-blockers. The study was published on September 23, 2105, in Diabetologia.
“Medications that block the renin-angiotensin-aldosterone system, such as ARBs and ACE inhibitors, had the strongest antidiabetic effect,” concluded lead author Ramón Hermida, PhD. “The RAAS follows a circadian rhythm, becoming active during sleep. Accordingly, in addition to BP-lowering, RAAS blockade might also serve as an effective strategy to control impaired glucose and insulin tolerance.”
RAAS is a hormone system that regulates BP and fluid balance. When renal blood flow is reduced, prorenin is converted into renin, cascading the release of angiotensin II, a potent vasoactive peptide that causes increased BP. Angiotensin II also stimulates secretion of aldosterone, which increases reabsorption of sodium and excretion of potassium, increasing the volume of extracellular fluid in the body, which also increases BP. Angiotensin II and aldosterone also contribute to increased hepatic glucose release and decreased insulin sensitivity.
Related Links:
University of Vigo
Researchers at the University of Vigo (Spain) conducted a prospective study involving 2,012 hypertensive patients (976 men, 1,036 women, and average age 53) without diabetes, who were randomized via a computer-generated allocation table to ingest their prescribed hypertension medications upon awakening or at bedtime. Investigators blinded to the hypertension treatment scheme of the patients then assessed the development of new-onset diabetes. Participants were followed for a mean 5.9 years.
The results showed that 171 participants developed type 2 diabetes during follow-up. Patients of the bedtime ingestion group showed significantly lower asleep BP and significantly lower risk of new-onset diabetes, after adjustment for fasting glucose, waist circumference, asleep systolic mean BP, dipping classification, and chronic kidney disease (CKD). The researchers observed greater benefit with medications that block the renin-angiotensin-aldosterone system (RAAS), such as angiotensin receptor blockers (ARBs), ACE inhibitors, and β-blockers. The study was published on September 23, 2105, in Diabetologia.
“Medications that block the renin-angiotensin-aldosterone system, such as ARBs and ACE inhibitors, had the strongest antidiabetic effect,” concluded lead author Ramón Hermida, PhD. “The RAAS follows a circadian rhythm, becoming active during sleep. Accordingly, in addition to BP-lowering, RAAS blockade might also serve as an effective strategy to control impaired glucose and insulin tolerance.”
RAAS is a hormone system that regulates BP and fluid balance. When renal blood flow is reduced, prorenin is converted into renin, cascading the release of angiotensin II, a potent vasoactive peptide that causes increased BP. Angiotensin II also stimulates secretion of aldosterone, which increases reabsorption of sodium and excretion of potassium, increasing the volume of extracellular fluid in the body, which also increases BP. Angiotensin II and aldosterone also contribute to increased hepatic glucose release and decreased insulin sensitivity.
Related Links:
University of Vigo
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