Naslov
Salt and renal vascular function

Autori
Drenjančević-Perić, Ines ; Lombard, Julian H.

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Final programme and abstract book of the 5th Central European Meeting on Hypertension & 2nd Croatian Congress on Hypertension & Croatian Meeting of Nurses in Hypertension : u: Hineka 9 (2009) / - Zagreb, 2009

Skup
Central European Meeting on Hypertension (5 ; 2009) ; Croatian Congress on Hypertension (2 ; 2009) ; Croatian Meeting of Nurses in Hypertension (2 ; 2009)

Mjesto i datum
Zagreb, Hrvatska, 22.10.2009. - 25.10.2009

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
dietary salt; renal vascular function

Sažetak
The most common environmental factor that contributes to the pathogenesis of hypertension is elevated dietary salt ingestion. It is well documented that high salt diet significantly affects the vascular function, leading to impaired vascular responses to various physiological and pharmacological stimuli, i.e. vasodilators and vasoconstrictors. The renal vasculature plays a major role in the regulation of renal blood flow and the ability of the kidney to control the plasma volume and blood pressure. Genetic and salt-sensitive hypertension is marked by renal vascular dysfunction, associated with renal vasoconstriction, increased vascular resistance, decreased renal blood flow, and consequent increase in plasma volume, and blood pressure. Although the mechanisms of dietary salt-induced hypertension and renal injury are still not clear, there is an increasing body of evidence that genetic mutations of sodium channels and related proteins, membrane ion transporter(s), and/or a regulatory enzyme in the nephron and renal vasculature are important in development of renal vascular dysfunction resulting in hypertension. In addition, vascular inflammation, and oxidative stress further promote renal vascular dysfunction, demonstrated as decrease in production/bioavailability of vasodilatory mediators (nitric oxide, prostaglandins, endothelium- derived hyperpolarizing factors) and/or increase in vasoconstrictors (such as tromboxane A2, endothelin, angiotensin II, 20-HETEs). Also, long-term HS diet induces renal injury and hypertension, which are associated with decreased renal VEGF expression. Modification of extracellular matrix composition could also lead to renal vascular remodeling and development of hypertension. In conclusion, reduction in dietary salt intake could be beneficiary in decreasing risk of renal damage and in management of hypertension.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti

POVEZANOST RADA