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At least 19 recordsLinked to original sources
PubMed2002

Diaphragm arterioles are less responsive to alpha1- adrenergic constriction than gastrocnemius arterioles.

The sympathetic nervous system has greater influence on vascular resistance in low-oxidative, fast-twitch skeletal muscle than in high-oxidative skeletal muscle (17). The purpose of this study was to test the hypothesis that arterioles isolated from low-oxidative, fast-twitch skeletal muscle [the white portion of gastrocnemius (WG)] possess greater responsiveness to adrenergic constriction than arterioles isolated from high-oxidative skeletal muscle [red portion of the gastrocnemius muscle (RG) and diaphragm (Dia)]. Second-order arterioles (2As) were isolated from WG, RG, and Dia of rats and reactivity examined in vitro. Results reveal that Dia 2As constrict less to norepinephrine (NE) (10(-9) to 10 (-4) M) than 2As from RG and WG, which exhibited similar NE-induced constrictions. This difference was not endothelium dependent, because responses of denuded 2As were similar to those of intact arterioles. The blunted NE-induced constrictor response of Dia 2As appears to be the result of differences in alpha1-receptor effects because 1) arterioles from Dia also responded less to selective alpha1-receptor stimulation with phenylephrine than RG and WG arterioles; 2) arterioles from Dia, RG, and WG dilated similarly to isoproterenol (10(-9) to 10(-4) M) and did not respond to selective alpha2-receptor stimulation with UK-14304; and 3) endothelin-1 produced similar constriction in 2As from Dia, RG, and WG. We conclude that differences in oxidative capacity and/or fiber type composition of muscle tissue do not explain different NE responsiveness of Dia 2As compared with 2As from gastrocnemius muscle. Differences in alpha1-adrenergic constrictor responsiveness among arterioles in skeletal muscle may contribute to nonuniform muscle blood flow responses observed during exercise and serve to maintain blood flow to Dia during exercise-induced increases in sympathetic nerve activity.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1989

Variations in arterioles in spontaneously hypertensive rats. Morphometric analysis of afferent and efferent arterioles.

In the present study, the diameters of afferent and efferent arterioles of kidneys from spontaneously hypertensive rats (SHR) were evaluated and compared with those from Wistar Kyoto rats. (WKY) using a vascular cast model. At 4 weeks of age, the blood pressure was slightly higher in SHR than in WKY (124 +/- 1 vs 116 +/- 7 mmHg, ns). The diameters of afferent arterioles in SHR were smaller than those in WKY (10.3 +/- 0.6 vs 12.3 +/- 0.7 microns, P less than 0.001), whereas the diameters of efferent arterioles were comparable in the two strains. At 20 weeks of age, the blood pressure was markedly elevated in SHR than in WKY (192 +/- 5 vs 140 +/- 4 mmHg, P less than 0.001). The diameters of afferent arterioles in SHR at this age were much smaller than those in WKY (14.3 +/- 0.5 vs 17.1 +/- 0.6 microns, P less than 0.01). The diameters of efferent arterioles in SHR were, however, larger than those in WKY (15.4 +/- 1.2 vs 12.9 +/- 0.4 microns, P less than 0.05). The net effect of these changes in arteriolar size helps to maintain normal intraglomerular pressure and to protect glomeruli from damage due to hypertension.

Aging↗
PubMed2001

Efferent arteriole tubuloglomerular feedback in the renal nephron.

BACKGROUND: Afferent and efferent arteriole resistance exerts critical and opposite actions in the regulation of glomerular capillary pressure (PGC) and glomerular filtration rate (GFR). Tubuloglomerular feedback (TGF) plays an important role in the regulation of afferent arteriole resistance; however, the role of TGF in the regulation of efferent arteriole resistance is less well established. We hypothesized that TGF caused by increased NaCl in the tubular fluid stimulates the macula densa to initiate a cascade of events resulting in efferent arteriole vasodilation, mediated by adenosine via its A2 receptor. METHODS: Rabbit efferent arterioles and adherent tubular segments with macula densa were simultaneously microperfused in vitro while changing NaCl concentration at the macula densa. To study whether autacoids produced by the glomerulus participate in the effect of TGF on efferent arterioles, they were perfused orthograde or retrograde. To eliminate the hemodynamic influence of the afferent arteriole during orthograde perfusion, the perfusion pipette was advanced to the distal end of the afferent arteriole, and the tip of the pressure pipette was placed beyond the afferent arteriole; for retrograde perfusion, the efferent arteriole was perfused from its distal end. RESULTS: In efferent arterioles perfused orthograde and preconstricted with norepinephrine (NE), increasing NaCl concentration at the macula densa increased the diameter by 33%. In preconstricted efferent arterioles perfused retrograde, increasing NaCl at the macula densa increased the diameter by 33%. Efferent arteriole vasodilation was completely blocked by a selective adenosine A2 receptor antagonist (3, 7-dimethyl-1-propargylxanthine) but not by an adenosine A1 receptor antagonist (FK838). CONCLUSIONS: Our data show that in vitro, preconstricted efferent arterioles dilate in response to increased macula densa NaCl, and this process is mediated by activation of adenosine A2 receptors. Thus, TGF changes efferent arteriole resistance in the opposite direction from the afferent arteriole, possibly amplifying TGF regulation of PGC and GFR. In vivo efferent arteriole TGF may only buffer the signals that cause efferent arteriole resistance to parallel changes in afferent arteriole resistance. Effects of TGF on efferent arterioles perfused orthograde or retrograde were similar, suggesting that glomerular autacoids do not participate in this process.

Animals↗
PubMed1998

Effect of betaxolol, timolol and nimodipine on human and pig retinal arterioles.

This study tested the hypothesis that the beta-adrenergic antagonists betaxolol and timolol, cause retinal arteriolar vasodilatation in addition to their ability to reduce intraocular pressure (IOP), and compared their vasodilatory ability with that of a known Ca2+ channel entry blocker nimodipine in donor human and pig isolated perfused retinal arterioles. This study was performed using a microperfusion technique specifically established to allow investigations in arterioles as small as the first order human and pig retinal arterioles (approximately 100 microns diameter). The scarcity of viable human tissue was overcome by the successful development of controlled rate freezing and cryopreservation techniques which were able to preserve the vascular responsiveness of the retinal arterioles, thus enabling multiple experiments to be performed on segments of retinal arterioles from each individual donor eye. Furthermore, relaxation by acetylcholine in noradrenaline contracted pig retinal arterioles showed that endothelial cell function was well maintained after cryopreservation (n = 8). Baseline diameters of retinal arterioles used in the main studies were: cryopreserved human 92.3 +/- 3.4 microns (n = 44), fresh pig 94.7 +/- 2.2 microns (n = 42), and cryopreserved pig 94.3 +/- 2.3 microns (n = 30). Precontraction with extraluminal endothelin-1 (ET-1) 10(-9) M reduced the diameters to 74.3 +/- 0.9%, 71.6 +/- 1.6% and 72.5 +/- 0.9% respectively. Intraluminally applied nimodipine and betaxolol caused a significant dose dependent dilatation (P < 0.001) in human retinal arterioles with a threshold of 10(-12) M. Timolol did not produce a significant dilatation in human arterioles. Timolol produced a small but significant dilatation in fresh and cryopreserved pig arterioles but the dilatation with betaxolol and nimodipine was significantly larger. The nimodipine and betaxolol dose response curves were not significantly different in human arterioles, but nimodipine produced significantly greater dilatation than betaxolol (P < 0.001) in fresh and cryopreserved pig arterioles. Both nimodipine and betaxolol were significantly more effective vasodilators than timolol (P < 0.001) in human and pig retinal arterioles.

Adrenergic beta-Antagonists↗
PubMed1998

Adaptation of flow-induced dilation of arterioles to daily exercise.

We aimed to test the hypothesis that daily exercise elicits an adaptation of blood flow/shear stress-induced dilation of arterioles. To this end we investigated the responses of isolated, pressurized arterioles of mesentery (MES) and plantaris (PL) skeletal muscle of sedentary (SED) and exercised (EX) rats to increases in perfusate flow (PF, range 0-30 microl/min). Rats were run on a treadmill, once daily for 3 to 4 weeks (with gradually increasing intensity up to 40 min at 28 m/min; a total of 15-19 sessions on the treadmill). The passive diameters of arterioles (obtained in Ca2+-free solution) were similar ( approximately 140 microm) but the pressure-induced active diameter (at 80 mmHg) of skeletal muscle arterioles was significantly smaller than that of mesenteric arterioles. The basal diameter of MES arterioles of SED and EX rats was: 83.5 +/- 3.6 and 83.9 +/- 2.9 microm, respectively; increases in PF increased the diameter of SED and EX arterioles to a similar degree by 33.2 +/- 4. 7 and 31.9 +/- 6.1 microm, respectively). The diameters of PL muscle arterioles of SED and EX rats were 62.1 +/- 6.2 and 68.0 +/- 5.5 microm. In contrast to arterioles of MES, the highest PF increased the diameters of arterioles of PL muscle from EX rats to a significantly greater extent than those from SED rats (52.4 +/- 7.8 vs 30.3 +/- 3.9 microm). Thus, there is a functional adaptation to exercise activity in arterioles of skeletal muscle but not in those of arterioles of mesentery. We speculate that the intermittent increase in blood flow/shear stress in arterioles of skeletal muscle during the periods of exercise activity may be the underlying mechanism responsible for this adaptation.

Adaptation, Physiological↗
PubMed1995

The mechanics of arteriole-tissue interaction.

Arterioles are embedded in the extensive connective tissue matrix of the interstitium. Mechanical interactions with the interstitium may affect the length-tension characteristics of arterioles, and thus affect their reactivity. However, no studies have adequately characterized the coupling between arterioles and the interstitium or investigated how the interstitium might change the physiological expression of arterioles. Therefore, the goal of this project was to investigate the mechanical interactions between arterioles and the interstitium and then to predict the physiological consequences of these interactions. We measured in situ the mechanical coupling of arterioles to the interstitium, the mechanical properties of the interstitium, and the structure of the interstitium in the hamster cheek pouch. We demonstrated that there are mechanical interactions between arterioles and the interstitium that are mediated both through direct connections and through the movement of extracellular fluid through the connective tissue network. We also found that the elastic modulus of the interstitium increases in the vicinity of the arteriole. Finally, both the mechanical coupling of arterioles to the interstitium and the mechanical properties of the interstitium are explained by the structure of the connective tissue matrix. The arterioles appear to be connected to adjacent fibroblasts and fibrocytes by collagen fibrils. These cells are in turn connected to the fiber matrix of the interstitium. Furthermore, the presence of these cells may explain the mechanical heterogeneity of the interstitium. We propose that the physiological role of the interstitium surrounding arterioles is to protect arterioles from stretching and deformation of the tissue while allowing these vessels to constrict freely.

Animals↗
PubMed1988

Myogenic activity in isolated subepicardial and subendocardial coronary arterioles.

The goal of this study was to examine myogenic responses of isolated porcine subepicardial and subendocardial arterioles (80-100 micron in diameter) within physiological ranges of intraluminal pressure. Arterioles were located by perfusion with india ink-gelatin solution then dissected and cannulated with glass micropipettes. Intraluminal pressure was altered in 20-cmH2O steps over the range of 20-140 cmH2O. IN physiological salt solution (36-37 degrees C), the coronary arterioles developed spontaneous tone and exhibited myogenic responses. At the lower pressures (20-60 cmH2O), subendocardial arterioles responded passively (diameter decreased from a control diameter at 60 cmH2O), whereas subepicardial arterioles maintained their diameters. At higher pressures (100-140 cmH2O), both subepicardial and subendocardial arterioles demonstrated myogenic constriction, but subepicardial arterioles demonstrated greater myogenic constriction than subendocardial arterioles. This implies that myogenic autoregulation in subepicardial arterioles is better than that in the subendocardial arterioles at both low and high pressures. In the presence of nitroprusside (10(-4) M), all arterioles responded to pressure changes passively, and there were no differences between subepicardial and subendocardial vessels. The functional integrity of the endothelium was verified by relaxation to substance P (10(-7) M). This is the first in vitro study to demonstrate coronary myogenic activity and transmural differences in these arteriolar responses. Our data support the concept that myogenic mechanisms in 80 to 100-micron arterioles may actively contribute to autoregulation of coronary blood flow.

Animals↗
PubMed1999

Role of NO and K(+)(ATP) channels in adenosine-induced vasodilation on in vivo canine subendocardial arterioles.

Adenosine (Ado) plays an important role in regulation of coronary vascular tone with nitric oxide (NO) and ATP-sensitive K(+) (K(+)(ATP)) channels. In vitro, it was reported that subendocardial (Endo) arterioles are more sensitive to Ado than subepicardial (Epi) arterioles. The purpose of this study was to observe enhanced vasodilation of Endo arterioles directly and to evaluate possible roles of K(+)(ATP) channels and NO in the different responses of Endo and Epi arterioles to Ado-induced vasodilation. We evaluated dilation of Endo and Epi arterioles (<120 micrometer) of beating canine hearts (n = 19) by Ado (20 and 50 microgram. kg(-1). min(-1) ic) before and after K(+)(ATP) channel blockade (glibenclamide; 200 microgram/kg ic), inhibition of NO synthase [N(G)-nitro-L-arginine methyl ester (L-NAME); 30 microgram. kg(-1). min(-1), 20 min ic], or glibenclamide + L-NAME using a novel needle-probe CCD intravital microscope. Ado induced dose-dependent vasodilation in both Epi and Endo arterioles, but vasodilation was greater in Endo arterioles, i.e., increase at 120 s (maximum dilation) after Ado (50 microgram. kg(-1). min(-1)) was 17% in Endo and 13% in Epi arterioles (P < 0.01). Endo arteriole dilation was attenuated by blockade of K(+)(ATP) channels from 18% (Ado) to 9% (Ado+glibenclamide) increase (P < 0.001) and by inhibition of NO synthase from 17% (Ado) to 9% (Ado+L-NAME) (P < 0.005). Epi arteriole vasodilation was attenuated by blockade of K(+)(ATP) channels from 15 to 9% (P < 0.005) and inhibition of NO from 16 to 10% (P < 0.005). Suppression of vascular response was additive (Endo, 14 to -1%; Epi, 12 to 3%) with glibenclamide + L-NAME. We conclude that 1) the degree of Ado-induced vasodilation was greater in Endo than in Epi arterioles, with higher sensitivity of smaller arterioles in both layers and 2) transmural difference of arteriolar sensitivity to adenosine was abolished or reversed by K(+)(ATP) channel blockade and/or by NO synthase inhibition, indicating crucial involvement of K(+)(ATP) and NO in transmural sensitivity difference.

Adenosine↗
PubMed1988

Carbon dioxide exchange across the walls of arterioles: implication for the location of the medullary chemoreceptors.

The location of the medullary chemoreceptors is not conclusively established. The original experiments, which were believed to suggest a shallow surface location in the ventrolateral medulla, have been questioned because substances, particularly CO2, applied on the surface of the medulla could diffuse into small arterioles. Because the whole tissue blood flow is supplied by surface arterioles, they could transport substances from the surface into the tissue to the respiratory centers. We studied simple transport equations describing movement of CO2 in arterioles bathed by rapidly flowing cerebrospinal fluid (CSF) and arterioles in tissue perfused by capillaries. Substantial exchange of CO2 could occur across the arteriole wall for all expected sizes of vessels when the partial pressure of CO2 at the outside wall was determined by CSF. When an arteriole is surrounded by tissue, only vessels with inside diameters (ID) less than or equal to 50 micron will exchange substantial amounts of CO2 but the smallest arterioles may be nearly in equilibrium with the tissue. The CO2 gradient in tissue around the arteriole will extend approximately 1 mm. Our simple theoretical description of CO2 transport in arterioles predicts substantial exchange in precapillary vessels. CO2 picked up by the smallest surface arterioles when the medulla is perfused at a high rate with CSF will not stay in the blood past the putative depth of the chemoreceptors. In arterioles greater than 30 micron, however, the CO2 could be carried to the respiratory centers.

Arterioles↗
PubMed1987

The response of arterioles in skeletal muscle grafts to vasoactive agents.

Arteriolar responses to the vasodilator adenosine and to the vasoconstrictor norepinephrine (NE) were examined in small bundles of extensor digitorum longus muscle grafted onto the cheek pouches of hamsters. Responses of arterioles to topically applied adenosine or NE were measured from 30 to 180 days after grafting and compared with the response of arterioles in control cheek pouches. Verapamil and potassium chloride (KCl) were applied to 120- and 180-day grafts to determine the response of arterioles to vasoactive agents not mediated by receptors. Arterioles in grafted muscle did not respond to adenosine until 60 days. The response increased with time but was significantly less than the control value even after 180 days. Arterioles in grafts did not respond to NE until 90 days. At both 90 and 120 days the degree of constriction in response to NE was not uniform along the length of a given arteriole (punctate response). By 180 days, the response of a given arteriole to NE was uniform but significantly less than the control value. In 120- and 180-day grafts the responses of arterioles to verapamil and KCl were similar to the responses of arterioles to adenosine and NE, respectively. We conclude that the diminished response of arterioles in small EDL muscle grafts to vasoactive agents may be caused by either a structural or a functional impairment in the smooth muscle layer of arterioles.

Adenosine Diphosphate↗
PubMed1994

Cell calcium concentration in glomerular afferent and efferent arterioles under the action of noradrenaline and angiotensin II.

The glomerular arterioles in the juxtaglomerular apparatus seem to function as effectors of the tubuloglomerular feedback mechanism. In this mechanism increased delivery of fluid to the distal nephron activates the macula densa cells through transport via an Na-2Cl-K cotransporter. This activation may lead to vasoconstriction of the afferent arteriole. Furthermore, vasoactive substances seem to affect both afferent and efferent arterioles. There are morphological differences along the afferent arteriole, some parts containing epithelioid cells with renin granules and others regular smooth muscle cells. The aim of the present experiments was to determine whether noradrenaline (10(-6) M) and angiotensin II (10(-6) M) had differential effects on the cell calcium concentration [Ca2+]i and on contraction in isolated perfused afferent and efferent arterioles and in the mesangial region. [Ca2+]i was measured with fura-2, an intensified videocamera and a digital imaging system. From the proximal to the distal part of the arteriole [Ca2+]i increased from about 100 to 250 nM. A [Ca2+]i increase and a contraction were caused by noradrenaline alone in the proximal part of the afferent arteriole and by angiotensin II alone in the distal part of this arteriole. In the mesangial region there was a high basal [Ca2+]i but no response to the vasoactive substances. In the efferent arteriole, application of both noradrenaline and angiotensin II led to an increase in [Ca2+]i and a contraction. The present experiments indicate that the two vasoactive substances tested act in a similar fashion along the whole length of the efferent arteriole, while in the afferent arteriole their actions are not equally distributed.

Angiotensin II↗