Neural Mechanisms in Hypertension

Brody, Michael J.; Haywood, Joseph R.; Touw, Kenneth B.

doi:10.1146/annurev.ph.42.030180.002301

Cited by 109 publications

(31 citation statements)

References 40 publications

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“…34 The relationship of these mechanisms to the observed microvascular changes require further systematic investigations and cannot be determined in the present study. A second possibility is that the observed diameter reductions may represent a microvascular process that is secondarily the result of hypertension and not the cause of hypertension.…”

mentioning

confidence: 80%

Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats.

Meininger¹,

Harris²,

Joshua³

1984

Hypertension

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SUMMARY Studies were performed on the cremaster skeletal muscle in rats to investigate the microvascular changes that are associated with established one-kidney, one clip (1K1C) and twokidney, one clip (2K1C) Goldblatt hypertension and with deoxycorticosterone (DOC)-salt hypertension. Rats were anesthetized with urethane and chloralo.se; and cremaster muscles with intact circulation and innervation were suspended in a controlled Krebs bath. Microvascular pressures and vessel diameters were measured at three consecutive arteriolar (A) and venular (V) branch levels. Arteriolar diameters (X ± SEM) in normotensive (NT) rats were 119 ± 7, 86 ± 5, and 31 ± 3 /xm respectively for 1A, 2A, and 3A arterioles; and venule diameters were 218 ± 12, 141 ± 15, and 53 ± 7 pun respectively for IV, 2V, and 3V venules. As compared to NT rats, there was a selective decrease in lumen size (percent reduction from control) for 1A and 2A (23% to 38%) in 1KIC and 2K1C rats and for 1A, 2A, and 3A (42% to 44%) in DOC rats. Venule diameters were not significantly different between normotensive and hypertensive animals at any branch level. Femoral artery pressures were significantly elevated (3= 43%) in all three forms of hypertension; however, this increase in pressure was not proportionally transmitted throughout the microcirculation. This was evidenced by normal pressure in 3A arterioles and in all venules for 1K1C and 2K1C rats and by normal pressures in 3V and larger venules for DOC rats. Our findings indicate that elevated arterial pressure in chronic renal hypertension is not transmitted uniformly across all microvascular segments. Furthermore, our data indicate that there is a selective increase in resistance for larger cremasteric arterioles and that a substantial increase in resistance occurs in those arterioles (> 100 fim diameter) located proximal to the cremaster microcirculation. (Hypertension 6: 27-34, 1984) KEY WORDS • microcirculation • renal hypertension • mineralocorticoid hypertension intravascular pressures T HE microcirculation plays a dominant role in the control of peripheral resistance and is therefore a good location in which to study factors or phenomena that might alter total peripheral resistance. Arterial hypertension is one well-known cardiovascular phenomenon in which total peripheral resistance is elevated.1 -2 Yet, little is known about the microvascular changes that contribute to the elevated peripheral resistance in hypertension. More detailed studies of the microvascular changes that accompany hypertension may provide valuable etiologic clues by

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confidence: 80%

Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats.

Meininger¹,

Harris²,

Joshua³

1984

Hypertension

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“…The following studies were aimed at addressing this issue by microinjecting selective opiate receptor ligands into a discrete hypothalamic region (nucleus preopticus medialis; POM) known to play an important role in cardiovascular control (Brody, Haywood & Tuow, 1980), and in which the presence of opioid peptides and receptors have already been established (Goodman etal., 1980;Law, Loh & Li, 1979 (YSI,model 73A). The arterial line was attached to a Narco microtransducer (RP 1500i) for blood pressure and heart rate recording; respiratory rate and relative pneumatic impedance (RPI) were recorded by subcutaneous electrodes through a Narco RPI coupler (type 7212).…”

Section: Introductionmentioning

confidence: 99%

Hypothalamic regulation of the cardiovascular and respiratory systems: role of specific opiate receptors

Faden

Feuerstein

1983

British J Pharmacology

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“…2 Other investigators have shown that the height of the systolic blood pressure correlates with the concentration of NE in the CSF compartment. 3 From experiments in animals, we have learned that surgical 4 ' 5 or chemical 6 ' 7 interruption of cardiovascular pathways either effectively prevents the development of high blood pressure, or alternatively, causes a remission of the hypertensive process. Last, but not least, delivery of either adrenolytic compounds 6 " 9 or blockers of the renin-angiotensin system 10 …”

mentioning

confidence: 99%

Neurogenic actions of angiotensin II.

Ferrario¹

1983

Hypertension

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Neural Mechanisms in Hypertension

Cited by 109 publications

References 40 publications

Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats.

Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats.

Hypothalamic regulation of the cardiovascular and respiratory systems: role of specific opiate receptors

Neurogenic actions of angiotensin II.

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