Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.

Grassı, Guıdo; Giannattasio, Cristina; Saino, Antonio; Sabadini, Ettore; Capozi, A; Sampieri, Lorena; Cuspidi, Cesare; Mancia, Giuseppe

doi:10.1161/01.hyp.11.1.92

Cited by 51 publications

(23 citation statements)

References 18 publications

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“…[15][16][17] Because cardiopulmonary receptors are sensitive to changes in central blood volume during both leg raising and lower body negative pressure, the alterations in cardiopulmonary receptor stimuli were assessed from the changes in left ventricular enddiastolic diameter. 18 The reflex responses were assessed from the changes in forearm circulation and plasma norepinephrine because of the major impact of cardiopulmonary receptor activity on both these variables. '5,1619 1224 Circulation Vol 82, No 4, October 1990 responsiveness to a neurogenic stimulus unrelated to that originating from cardiopulmonary receptors.20…”

Section: Methodsmentioning

confidence: 99%

Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

et al. 1990

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Cardiopulmonary receptor control of the circulation is impaired in a variety of diseases having cardiac hypertrophy as a common feature. Whether this also occurs in the so-called "physiological" cardiac hypertrophy of the athlete, however, is unknown. We studied nine sedentary healthy subjects and 19 age-matched professional runners or hammer throwers who had trained at least 2 hours per day, 5 days per week for 7 years. The left ventricular mass index (echocardiography) was 99±7.4 and 135+±5.9 g/m2 in the two groups, respectively. Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter for 5 minutes by leg raising and lower body negative pressure, keeping both stimuli at a level not affecting blood pressure and heart rate. In the sedentary healthy subjects, forearm vascular resistance (the ratio between mean arterial pressure and forearm blood flow) and plasma norepinephrine fell during leg raising (forearm vascular resistance, -7+1.7 units; norepinephrine, -57.4±1.4 pglml) and increased during lower, body negative pressure (forearm vascular resistance, 20±5.3 units; norepinephrine, 97.7+±21.5 pg/ml). For similar or greater alterations in left ventricular end-diastolic diameter, the correspondent changes observed in the professional runners or hammer throwers were -5.3±1.3 units (forearm vascular resistance), -35.4±9.6 pg/mI (norepinephrine), 9.1± 1.4 units (forearm vascular resistance), and 30.9±6.9 pg/ml (norepinephrine). This represented an attenuation of 25%, 38%, 55%, and 68%, respectively (p<0.01), of the control response. The attenuated response to lower body negative pressure was accompanied by a greater decline in arterial blood pressure during a more pronounced lower body negative pressure stimulus. In contrast, forearm vascular resistance responses to cold pressor test were similar in the professional runners or throwers and in the sedentary healthy subjects. Thus, the pronounced cardiac hypertrophy of professional athletes is accompanied by an impairment of the cardiopulmonary receptor reflex. This may lead to a reduced efficacy of cardiovascular homeostasis. (Circulation 1990;82:1222-1229 P revious studies have shown that the reflex alterations in sympathetic activity induced by nonhypotensive changes in central blood volume are markedly reduced in patients with heart transplantation, demonstrating their main origin from cardiac receptors.1-3 They have also shown that these alterations are slightly diminished in mild or moderate essential hypertension but that a pronounced reduction occurs when the hypertension is associated with cardiac hypertrophy. Thus, a pathological thickening of the heart impairs the cardiogenic reflex control of the cardiovascular system.4 Professional athletes often show a pronounced cardiac hypertrophy.5,6 Whether this leads to an impairment of the cardiovascular control originating from the cardiopulmonary region, however, is unknown. This is relevant to the debated question of whether the card...

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Section: Methodsmentioning

confidence: 99%

Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

et al. 1990

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“…22,23 When involvement of arterial baroreceptors is avoided, stimulation of cardiopulmonary receptors causes a general withdrawal of the sympathetic outflow, but the effect on renal sympathetic tone is most pronounced. Furthermore, it has been shown that cardiopulmonary receptors mediate systemic renin release through …”

Section: Sodium Sbp and Effective Total Vascular Compliancementioning

confidence: 99%

“…In subjects with mild-to-moderate essential hypertension, this reninreflex modulation remains operative but exerts reduced effectiveness compared with normal subjects. 22 Finally, in hypertensive subjects, total blood volume and effective compliance of the vascular bed are significantly reduced. In the presence of preserved cardiac performance, central venous pressure is increased slightly but significantly.…”

Section: Safar Et Al Sodium and Vascular Stiffness 205mentioning

confidence: 99%

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Sodium Intake and Vascular Stiffness in Hypertension

et al. 2009

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T he relationship between sodium and blood pressure (BP) continues to be the focus of intense research. In humans, the impact of sodium on systolic BP (SBP), diastolic BP (DBP), mean BP, and pulse pressure (PP) is currently thought to be quite similar for the 4 pressures and to occur practically with identical consequences (see reviews [1][2][3][4][5][6][7][8] ). In this review, the effect of sodium on SBP is taken into consideration mainly for a very simple but important reason: in recent years, SBP and PP have become the parameters the most difficult to control in hypertensive subjects, which is the principal goal of most antihypertensive drugs. 1 Central (aortic) SBP is a complex parameter that is influenced both by cardiac (stroke volume and ventricular ejection) and vascular (arterial and venous stiffness and wave reflections) factors. 1 Stroke volume, the ratio between cardiac output and heart rate, depends not only on cardiac structure and function but also on venous return. Through the extracellular and intravascular spaces and their elastic properties, stroke volume and, hence, SBP are strongly associated with sodium balance, ie, with the relationship between sodium intake and its urinary elimination, and, finally, the traditional pressure-diuresis mechanism. 4 This pathway, which mainly affects the venous circulation, requires a low and steady BP, together with a vast storage capacity for salt and water. Another important pathway affects the high-pressure pulsatile arterial system, in which the SBP level is achieved through increased arterial stiffness and disturbed wave reflections. These hemodynamic parameters are strongly influenced by sodium intake, and their anomalies are mostly seen in subjects Ͼ50 years old. 1,2,5,7,9 Note that, in humans, the volume and elasticity of the arterial space are very low compared with the corresponding values for the venous system. 1 We have 2 principal aims for this review. First, how does dietary sodium influence vascular stiffness and, through mechanisms affecting the venous circulation, modulate stroke volume and SBP, potentially leading to hypertension? Second, how does sodium intake adversely affect the arterial circulation and, through increased arterial stiffness and wave reflections, potentially worsen hypertension and exacerbate cardiovascular risk? These 2 questions are detailed successively after a brief historical review of the traditional relationships between sodium and BP and a summary of their interactions with the renin-angiotensin-aldosterone system (RAAS). Other hormonal factors, with the exception of antidiuretic hormone, are beyond the scope of this review. Sodium, SBP, and Cardiovascular Risk: A Brief Historical OverviewOver the last few decades, a considerable body of evidence has shown major links along with cause-and-effect relationships between salt intake and BP. They have given rise to numerous publications and reviews, summarized here. [1][2][3][4][5][6][7][8] In most studies, SBP and DBP were considered to be equivalent mechanical facto...

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“…TM In addition to modulating the neural response to orthostatic stress, it has also been demonstrated that in healthy man cardiopulmonary baroreceptors modulate renin release. 19 There are other receptors located within the ventricle; these stretch receptors have recently been shown to be important in modulating changes in forearm vascular resistance in response to changes in pressure. 2~ High pressure mechanoreceptors are situated in the walls of the aortic arch and in the carotid sinus; these stretch receptors have nerve endings embedded in the adventitial layer of the arterial wall.…”

Section: Discussionmentioning

confidence: 99%

A carbohydrate meal attenuates the forearm vasoconstrictor response to lower body subatmospheric pressure in healthy young adults

Kearney

Stubbs

Cowley

et al. 1997

Clinical Autonomic Research

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The cardiovascular (CV) responses to meal ingestion and orthostasis are well established. The effect of meal ingestion and meal composition on the CV responses to orthostasis are unknown. The effect of high carbohydrate (HC) and high fat (HF) meal ingestion on the CV responses to simulated orthostatic stress (using graded lower body subatmospheric pressure (LBSP)) was assessed in nine healthy young volunteers. Cardiac output (CO), forearm blood flow (FABF) heart rate (HR) and blood pressure (BP) were measured before and during LBSP while fasted and after eating HC and HF meals. Ingestion of both meals led to an increase in CO and HR. Both meals resulted in a fall in total peripheral resistance but only HC led to a significant fall in BP (p < 0.05). HF had no effect on the CV responses to LBSP, whereas HC resulted in attenuated FABF and forearm vascular resistance responses (p < 0.05). Thus, ingestion of an HC meal significantly attenuates the forearm vascular response to orthostatic stress and the hypotensive effect of orthostasis is additive to that occurring after an HC meal.

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Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.

Cited by 51 publications

References 18 publications

Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

Sodium Intake and Vascular Stiffness in Hypertension

A carbohydrate meal attenuates the forearm vasoconstrictor response to lower body subatmospheric pressure in healthy young adults

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