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The effect of high NaCl diet on resistance arteries is not yet fully documented. In order to assess the effect of NaCl on myogenic tone and flow-induced dilation independent of arterial blood pressure change, we used normotensive rats which did not develop hypertension upon high NaCl intake. Normotensive Wistar Kyoto Rats received a high (8%) or a normal NaCl diet (0.4%). Mesenteric resistance arteries (150 microm, internal diameter) were cannulated in an arteriograph to allow perfusion of arteries under controlled pressure and flow. Pressure-induced myogenic tone was lower in the high NaCl group than in the control group. Cyclooxygenase inhibition with indomethacin and (N-(2-cyclohexyloxy)-4-nitro-phenyl)-methanesulphonamide, 1 micromol/l) NS 398 (specific cyclooxygenase-2 inhibitor) similarly decreased myogenic tone in rats fed high NaCl but had no effect in those fed a normal NaCl diet. Flow-induced dilation was decreased in the high NaCl group. Inhibition of nitric oxide synthesis with N(G)-nitro-L-arginine methyl ester decreased flow-induced dilation in both groups. Indomethacin and NS 398 did not change flow-induced dilation. As shown by immunofluorescence COX-2 was present in the endothelium of arteries from rats with a high NaCl diet but not in those fed a normal NaCl diet. Thus, chronic high NaCl intake decreased both flow-induced dilation and myogenic tone in resistance arteries. The chronic high NaCl did not affect the participation of nitric oxide on flow-induced dilation, but induced the expression of cyclooxygenase-2, which participates in myogenic tone. These results suggest that high NaCl changes flow and pressure mechanosensing processes and strengthen the hypothesis that sodium ions have an important role in both pressure and flow-mechanotransduction in vascular cells.

We investigated the effect of prolonged endothelin-1 type A (ET(A)) receptors blockade on the constrictor response to phenylephrine and the dilator response to acetylcholine (ACh) in isolated aortic rings from normotensive [Wistar-Kyoto (WKY)] rats and spontaneously hypertensive rats (SHRs). Animals were treated for 2 weeks with the ET(A)-receptor blocker LU135252 (50 mg/kg/day; n = 8). LU135252 treatment did not affect blood pressure in both strains. In isolated aortic segments, dilation to ACh and contractions to phenylephrine were decreased only in SHRs. Nitric oxide (NO) synthesis blockade (L-NAME, 0.1 mM) inhibited 90+/-11% (WKY rats) and 76+/-8% (SHRs) of ACh-induced dilation. Cyclooxygenases blockade (indomethacin, 10 microM) had no effect in both strains. Endothelium-derived hyperpolarizing factor(s) (EDHF) blockade (KCl, 20 mM) suppressed the remaining ACh-induced dilation in both strains. Treatment with LU135252 significantly decreased NO-dependent dilation, as compared with controls [70+/-8% vs. 90+/-11% (WKY rats) and 54+/-6% vs. 76+/-8% (SHRs) of total dilation; p<0.05]. On the other hand, EDHF-dependent dilation was significantly higher in the LU135252 groups [29+/-5% vs. 10+/-3% (WKY rats) and 44+/-7% vs. 19+/-4% (SHRs) of total dilation; p<0.05]. Thus prolonged ET(A)-receptor blockade decreased the responsiveness to phenylephrine and ACh in SHR aortas and changed the proportion of dilator agents in ACh-induced dilation.

Objective: To compare the mechanical properties of carotid arteries from normotensive and spontaneously hypertensive rats., Design: The pressure-diameter relationships of carotid arteries from nine normotensive adult Wistar-Kyoto (WKY) and nine spontaneously hypertensive rats (SHR) were measured in vitro under control conditions and after poisoning the smooth muscle cells with potassium cyanide., Methods: Changes in diameter due to changes in transmural pressure were determined with an ultrasonic dimensiometer (12 MHz). The diameter values were determined from the transit times of the pair of echoes given by the proximal and distal walls. The carotid artery was submitted to stepwise increases in pressure of 25 mmHg, from 0 to 200 mmHg; each pressure level was maintained for 5 min before the arterial diameter was recorded., Results: The carotid artery pressure-diameter relationship was a sigmoid curve in both strains. At the same level of pressure, the diameter of the carotid artery from SHR was significantly larger than that from normotensive rats (P < 0.05). Furthermore, the diameter values measured at the operating mean arterial pressure (roughly 100 mmHg for WKY rats and 150 mmHg for SHR) were markedly different (P < 0.001). In both strains, the diameter under passive conditions (with potassium cyanide) was significantly larger than that measured under control conditions (P < 0.01)., Conclusions: Carotid arteries from SHR were significantly stiffer than those from WKY rats. Due to the pressure-dependency of the arterial wall stiffness, the increased arterial stiffness reported in hypertensive rats in vivo is related to an increase in distending arterial pressure and also to a significant reduction in the intrinsic compliance of the arterial wall.

Aim: To measure the mechanical properties of the rat carotid artery as affected by physiological and pharmacological changes., Methods: We used an in situ measurement method that did not affect the anatomy, vascularization or innervation of the carotid artery, in normotensive and in spontaneously hypertensive rats (SHR), to evaluate the effects of ageing, hypertension and acute or chronic drug-induced vasorelaxation., Results: The compliance-pressure curve was characterized, under baseline conditions, by two phases, an ascending component in the lower pressure ranges and a descending component in the higher pressure ranges. In younger or older normotensive rats the maximum value of carotid compliance was observed for values of transmural pressure that approximated those of the operating mean blood pressure. For any given value of transmural pressure, carotid compliance was lower in the hypertensive rats, whether younger (3 months) or older (18 months), than in normotensive rats. This finding was particularly striking for transmural pressures below 125 mmHg, and held true even after the administration of potassium cyanide. Consequently, the reduced compliance in the hypertensive rats was attributed predominantly to structural changes in the arterial wall. Moreover, in the hypertensive rats there was a dissociation between the operating arterial blood pressure level and the maximum value of carotid arterial compliance. Thus in young SHR, whereas the operating systemic blood pressure was shifted toward higher values (> 175 mmHg), the maximum value of carotid compliance was observed for pressure levels close to 125 mmHg. This dissociation was more pronounced in older SHR (mean blood pressure 200 mmHg; maximum compliance 75 mmHg)., Conclusions: The acute administration of vasodilators or of potassium cyanide induces relaxation of vascular smooth muscle and increases compliance for distension pressures of up to 125 mmHg. Since the drugs had no effects on arterial compliance at higher pressure levels, we conclude that in SHR acute vasorelaxation can increase operating compliance only if blood pressure is reduced. In contrast, chronic treatment with vasodilating agents is able to increase compliance even for higher blood pressure levels. Therefore, we suggest that chronic treatment can improve the elastic properties of the arterial wall through changes in the arterial wall structure.

The high-pressure systemic arterial network plays a major physiological role as it buffers the impact of the blood flow wave generated by the left ventricle and transforms it into a more continuous flow in the peripheral arterioles. In ageing processes unrelated to hypertensive or vascular disease the structural properties of the arterial network are significantly altered. The collagen, elastin and smooth muscle contents of the tunica media and the geometrical arrangement of arterial wall components are constantly modified according to the subject's age. These morphometric changes are responsible for changes in the mechanical properties of the arterial walls leading to rigidity. An increase in caliber of the arterial lumen has been found in all studies; it partially compensates for the effects of arterial wall rigidity on vascular compliance, thereby limiting the haemodynamic and functional changes that occur in blood circulation.