Cellular mechanisms involved in the vascular myogenic response

Meininger, Gerald A.; Davis, Michael J.

doi:10.1152/ajpheart.1992.263.3.h647

Cited by 228 publications

(216 citation statements)

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“…(8,39,45). Those signal pathways may be involved in a myogenic response of the blood vessel (38,49). In the present study, we observed that the vessels incubated with apocynin could not develop mygenic tone in physiological loading at zero flow and remained at a significantly larger diameter than in the control, which is consistent with previous observations (49).…”

Section: Discussionsupporting

confidence: 93%

NADPH oxidase has a directional response to shear stress

Godbole¹,

Lu²,

Guo³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Godbole AS, Lu X, Guo X, Kassab GS. NADPH oxidase has a directional response to shear stress. Am J Physiol Heart Circ Physiol 296: H152-H158, 2009. First published November 14, 2008 doi:10.1152/ajpheart.01251.2007.-Vessel regions with predilection to atherosclerosis have negative wall shear stress due to flow reversal. The flow reversal causes the production of superoxides (O 2 Ϫ ), which scavenge nitric oxide (NO), leading to a decrease in NO bioavailability and endothelial dysfunction. Here, we implicate NADPH oxidase as the primary source of O 2 Ϫ during full flow reversal. Nitrite production and the degree of vasodilation were measured in 46 porcine common femoral arteries in an ex vivo system. Nitrite production and vasodilation were determined before and after the inhibition of NADPH oxidase, xanthine oxidase, or mitochondrial oxidase. NADPH oxidase inhibition with gp91ds-tat or apocynin restored nitrite production and vasodilation during reverse flow. Xanthine oxidase inhibition increased nitrite production at the highest flow rate, whereas mitochondrial oxidase inhibition had no effect. These findings suggest that the NADPH oxidase system can respond to directional changes of flow and is activated to generate O 2 Ϫ during reverse flow in a dose-dependent fashion. These findings have important clinical implications for oxidative balance and NO bioavailability in regions of flow reversal in a normal and compromised cardiovascular system. superoxide; nitric oxide; oxidative balance; reduced nicotinamide adenine dinucleotide phosphate NITRIC OXIDE (NO) is released by endothelial cells to regulate blood vessel diameter acutely as well as to maintain long-term homeostatic conditions of the vessel wall (4,30). NO is produced in the endothelium from L-arginine by the enzyme endothelial NO synthase (eNOS) (4, 41) and is released in response to endothelial shear stress and other stimuli such as acetylcholine (4). Wall shear stress (WSS) has also been found to regulate the activity and expression of eNOS (34,40).Oscillatory and reverse WSS have negative effects on the endothelium due to superoxide (O 2 Ϫ ) production (14, 27, 28, 36, 52). It has been found that reverse flow in blood vessels causes reduced NO due to increased O 2 Ϫ production (36). Since NO is atheroprotective, regions of oscillatory and reverse WSS are more prone to atherosclerosis. Regions near branch points and curved vessels produce near-wall reverse flow (15,16).O 2 Ϫ can quickly inactivate NO, causing reduced NO bioavailability and endothelial dysfunction (9, 33). This endothelial dysfunction is implicated in atherosclerosis, hypertension, and heart failure (9,13,14,18,21). Reduced NO in the vessel wall impairs endothelium-dependent vasodilation, decreases inhibition of platelet and leukocyte adhesion, and is linked to the development of intimal hyperplasia (4, 21, 51). Our group has previously shown that NO production is reduced during reverse flow and that the addition of Tempol (an O 2 Ϫ scavenger) restored NO production in reverse flow to...

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Section: Discussionsupporting

confidence: 93%

NADPH oxidase has a directional response to shear stress

Godbole¹,

Lu²,

Guo³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Transmembrane calcium entry into VSMC occurs mainly through voltage-operated calcium channels, which are considered to be essential for the myogenic control of vascular tone [14]. Our previous findings with L-type calcium channel antagonists also support a role for such channels in the autoregulation of renal blood flow [22].…”

Section: Discussionmentioning

confidence: 53%

“…Recent studies suggest that VSMC respond to membrane stretching with calcium entry through a dihydropyridineinsensitive mechanism [3]. The relevance of stretch-activated ion channels has also been considered for the myogenic regulation of vascular resistance [3,14]. Since juxtaglomerular cells reversibly differentiate from VSMC [2,25], one could speculate from our findings on whether the pressure control of renin release is mediated by a similar mechanism involving transmembrane calcium entry into renal juxtaglomerular cells through stretch-activated cation channels.…”

Section: Discussionmentioning

confidence: 67%

Role of calcium ions in the pressure control of renin secretion from the kidneys

Scholz

Hamann

et al. 1994

Pfl�gers Arch

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Abstract. In this study we examined the role of calcium ions in the control of renin release by the renal artery pressure. For this purpose renin secretion rates (RSR) were measured in isolated rat kidneys perfused at pressures of 140, 100, 80 and 40 mmHg [19,13,11, 5 kPa) with media containing either 1.5 retool/1 ("normal") or zero calcium concentrations (calcium-free perfusate with 0.5 mmol/1 EGTA). At normal calcium the RSR was inversely related to the renal artery pressure, whereas calcium withdrawal resulted in an almost linear and proportional relationship between RSR and perfusion pressure. As a consequence, RSR at 140 mmHg (19 kPa) with a calcium-free medium was similar to renin release at 40 mmHg (5 kPa) with normal calcium. The nitric oxide (NO) donor sodium nitroprusside (1 t~mol/1) stimulated RSR in a pressure-dependent fashion at a calcium concentration of 1.5 mmol/1. With a calcium-free perfusate, sodium nitroprusside did not restore the inverse pressure dependence of RSR seen with normal calcium but almost doubled the RSR across the whole pressure range. Whilst RSR was significantly reduced by angiotensin II (1 nmol/1) in the range between 40 mmHg and 140mmHg (5-19kPa) with normal calcium, withdrawal of extracellular calcium ions practically abolished the inhibitory action of angiotensin II. Since angiotensin II attenuated RSR especially at low renal perfusion pressure, our results indicate that renin release in this pressure range is still inhibitable by calcium mobilization in renal juxtaglomerular cells. Thus, the enhancement of renin secretion at lower pressures cannot be explained by a decreased sensitivity of renin release towards calcium ions. Instead, our data support the hypothesis that the "baroreceptor" control of renin secretion is maintained through a pressure-related calcium influx mechanism into juxtaglomerular cells which counteracts the stimulatory effect of locally released NO.

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“…Kleinhaus & Kao (1969) (Nakayama & Tanaka, 1993 Ca2P channels (Kirber et at. 1988;Meininger & Davis, 1992).…”

Section: Discussionmentioning

confidence: 99%

Stretch‐induced enhancement of contractions in uterine smooth muscle of rats.

Kasai

Tsutsumi

Taketani

et al. 1995

The Journal of Physiology

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1. We studied the effect of servo-controlled stretch of smooth muscle strips from rat uterus on tension and intracellular Ca2+ concentration ([Ca2+]i, using fura-2 as an indicator) at 300C. 2. When quiescent uterine muscle strips were stretched at a ramp time of 0 5 s by multiples of 5% of the resting muscle length (Lo) up to 40%, forty-two out of sixty muscle strips responded with a transient active contraction and a [Ca2+]i increase. The minimum excursion of stretch required for contraction was 26 3 + 7 5% of Lo (mean + S.D.). The peak response had an all-or-none property and was almost independent of the duration of stretch. 5. When a stretch of 15-35% of Lo was applied during the relaxation phase of 10 nM oxytocin-induced rhythmic contractions, the first contraction after the stretch occurred earlier than that expected from the control rhythm. However, the frequency of the subsequent rhythm returned to almost the control level even during continued application of stretch, although the half-width of rhythmic contractions was increased during stretch. 6. The present study demonstrates that stretch of uterine muscle induces a transient contraction due to Ca2+ influx, which is myogenic and dependent on the excursion and velocity of stretch. The all-or-none property of the stretch-induced contractions suggests initiation of Ca2+ spikes. Furthermore, stretch modulates the oxytocin-induced rhythmic contractions.

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Cellular mechanisms involved in the vascular myogenic response

Cited by 228 publications

References 0 publications

NADPH oxidase has a directional response to shear stress

NADPH oxidase has a directional response to shear stress

Role of calcium ions in the pressure control of renin secretion from the kidneys

Stretch‐induced enhancement of contractions in uterine smooth muscle of rats.

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