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Does Stress-induced Impaired Pressure Natriuresis Contribute To Renal Disease?

Date:
September 30, 2003
Source:
American Physiological Society
Summary:
Previously published studies indicate that the renal pressure natriuresis mechanism -- the excretion of abnormal amounts of sodium in the urine -- is abnormal in all forms of hypertension studied thus far. A team of researchers has examined whether this mechanism, when affected by stress, contributes to the development of renal disease in adolescents.

(Atlanta, GA) – Maintaining a healthy balance of fluids and sodium in our body is important. An intricate part of the balance involves a control system known as the "renal-pressure natriuresis mechanism." Previously published studies indicate that the renal pressure natriuresis mechanism -- the excretion of abnormal amounts of sodium in the urine -- is abnormal in all forms of hypertension studied thus far. A team of researchers has examined whether this mechanism, when affected by stress, contributes to the development of renal disease in adolescents.

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A New Study

The researchers are Coral Hanevold, Gregory Harshfield, Kathryn McLeod, Gaston Kapuku, Martha Wilson, Lynne Mackey, Delores Gillis and Lesley Edmunds, all of the Medical College of Georgia, Augusta, GA. They will present the results of their work, entitled, "Impaired Pressure Natriuresis and Renal Function in Adolescents" during the upcoming scientific conference, Understanding Renal and Cardiovascular Function Through Physiological Genomics, a meeting of the American Physiological Society (APS) (www.the-aps.org), being held October 1-4, 2003 at the Radisson Riverfront Hotel and Convention Center, Augusta, GA.

Methodology

The researchers examined changes in blood pressure (BP), urinary sodium excretion (UNaV), angiotensin II (Ang II) and urinary creatine (UCr) in 210 adolescents across a 5-hour test period. The period consisted of a 2-hour baseline, 1-hour stress period, and a 2-hour recovery period.

Blood pressure was obtained at 15-minute intervals and blood and urine samples were obtained hourly. The subjects were divided into those that increased (excreters: n=151) or decreased UNaV during stress (retainers: n=59). The groups were similar with respect to age, height, weight and casual BP.

Results

The researchers noted that:

the time by group interactions were significant for UNaV (P< 0.001) and UCr (P<0.03);

retainers continued to decrease UNv at 2 hours following stress;

UCr peaked during stress for both groups, but the change was greater for retainers (P<0.02), with a significantly higher level during stress (P< 0.006) that remained elevated until the last hour; and

the stress related increase in UCr was correlated with ANG II levels during stress (r=0.44:P<0.01). These patterns were coupled with higher levels of BP for retainers 2 hours following stress (113±10 versus 11±9 mmHg; P<0.05), despite similar levels prior to and during stress. Conclusions

The observed changes in UCr during and after stress, coupled with an extended period of relative hypertension post-stress, indicate that the workload of the kidney is excessive in subjects that show impaired stress-induced (i.e., retainers). These data indicate that this response pattern increases the load on the kidney, which may lead to the early development of renal disease.


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The above story is based on materials provided by American Physiological Society. Note: Materials may be edited for content and length.


Cite This Page:

American Physiological Society. "Does Stress-induced Impaired Pressure Natriuresis Contribute To Renal Disease?." ScienceDaily. ScienceDaily, 30 September 2003. <www.sciencedaily.com/releases/2003/09/030930054652.htm>.
American Physiological Society. (2003, September 30). Does Stress-induced Impaired Pressure Natriuresis Contribute To Renal Disease?. ScienceDaily. Retrieved March 27, 2015 from www.sciencedaily.com/releases/2003/09/030930054652.htm
American Physiological Society. "Does Stress-induced Impaired Pressure Natriuresis Contribute To Renal Disease?." ScienceDaily. www.sciencedaily.com/releases/2003/09/030930054652.htm (accessed March 27, 2015).

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