High Sodium Intake Decreases Pressure-Induced (Myogenic) Tone and Flow-Induced Dilation in Resistance Arteries From Hypertensive Rats

Abstract

Abstract-High sodium intake has been associated with a higher blood pressure level. Resistance arteries are the main determinants of blood pressure. They are largely regulated by pressure (tensile stress)-induced tone (myogenic tone, MT) and by flow (shear stress)-induced dilation (FD). Thus, we studied the effect of NaCl (8%) intake for 8 weeks on FD and MT in mesenteric resistance arteries of spontaneously hypertensive rats. Arteries were cannulated and mounted in an arteriograph. Intraluminal diameter was measured continuously. High NaCl intake increased mean arterial pressure (186Ϯ5 to 217Ϯ6 mm Hg, PϽ0.01). Passive arterial diameter ranged from 112Ϯ6 to 185Ϯ9 m (pressure from 25 to 125 mm Hg, no effect of NaCl). MT developed in response to pressure (tone from 89Ϯ1% to 83Ϯ3% of passive diameter, 25 to 125 mm Hg). High NaCl intake significantly decreased MT (89Ϯ1% versus 83Ϯ3% of passive diameter when pressure was 125 mm Hg, PϽ0.023). High NaCl intake also decreased FD (6.5Ϯ0.8 versus 10Ϯ1.3 m dilation under a pressure of 100 mm Hg and a flow rate of 160 L/min, PϽ0.012). Thus, high salt intake decreased both flow (shear stress)-induced dilation and pressure (tensile stress)-induced tone in mesenteric resistance arteries. These findings might reflect attenuation by NaCl of flow and pressure mechanosensor processes. (Hypertension. 1998; 32:176-179.)Key Words: myogenic tone Ⅲ shear stress Ⅲ blood vessels Ⅲ resistance arteries Ⅲ sodium F low (shear stress)-induced dilation and pressure (tensile stress)-induced tone (myogenic tone) are two fundamental mechanisms for the control of vascular tone. Shear stress is a potent stimulus for vascular endothelial cells, triggering the release of vasoactive agents such as nitric oxide (NO), cyclooxygenase products, hyperpolarizing factors, and contracting factors.

Endothelial basement membrane laminin 511 is essential for shear stress response

“…Hence, while there was no overt remodelling, such as increased collagen deposition and large changes in wall thickness (Mulvany, 1999), there were changes to the vessel dimensions to accommodate their inability to respond appropriately to changes in flow, as reported in other mice models (Albinsson et al , 2007). There are reports of altered shear response in resistance arteries of diabetic and hypertensive rats (Matrougui et al , 1998; Bouvet et al , 2007; Belin de Chantemele et al , 2009; Vessieres et al , 2012; Dumont et al , 2014) where expression or glycosylation state of extracellular matrix molecules is commonly affected (Intengan & Schiffrin, 2000; Rauch et al , 2011; Bogdani et al , 2014). However, there has been no investigation of whether changes in shear response in such pathological vessels are associated with changes in laminin isoform expression, a possibility that requires future investigation.…”

Angiotensin II Stimulates Extracellular Signal–Regulated Kinase Activity in Intact Pressurized Rat Mesenteric Resistance Arteries

“…11,12 The pressure myograph used in the present study contained 2 chambers and allowed vessel diameter to be measured online by use of a video-microscope arrangement. Each resistance artery was connected to a perfusion circuit consisting of a glass reservoir and a pressure chamber, allowing the control of hydrostatic pressure in the intraluminal compartment.…”

Activation of AT 2 Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries

“…Passive diameter was then determined. 13,[22][23][24] Results are given in micrometers for artery diameters and flow-induced relaxation. [22][23][24] In another series of experiments (nϭ6), angiotensin II (0.1 nmol/L) was perfused in mesenteric arteries after pretreatment of the vessels with the AT 1 receptor blocker candesartan cilexetil (10 nmol/L).…”