Pulmonary Hypertension

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As mentioned earlier, the AM peptide and mRNA are expressed in the lungs, where AM receptors are also detected (Owji et al., 1995; Kitamura et al., 2002). AM has been shown to dilate the pulmonary artery, thereby reducing pulmonary arterial pressure. To investigate the role of AM in pulmonary hypertension, Shimokubo et al. (1995) measured the plasma levels of AM in rats with monocrotaline-induced pulmonary hypertension. The plasma AM levels in this model were found to be higher than those in control rats. Nakanishi et al. (2004) found that AM mRNA and peptide were upregulated in the right ventricle and lungs of rats with pulmonary hypertension induced by hypobaric hypoxia. In addition to the upregulation, gene expression of the AM receptor components was found to be augmented in hypoxic rat lung (Qing et al., 2001). Kakishita et al. (1999) reported the plasma AM levels in patients with primary pulmonary hypertension or pulmonary hypertension secondary to chronic thromboembolism. In accord with the animal study, the AM levels in these patients were elevated compared to those of controls, and the increase was related to an elevation of mean pulmonary arterial pressure, right atrial pressure and pulmonary arterial resistance. These findings suggested AM acts against the elevation of pulmonary arterial pressure.

Yoshihara et al. (1998) reported the effects of continuous, subcutaneous administration of AM for three weeks in monocrotaline-induced pulmonary hypertension in rats. In their intervention experiments, AM partially inhibited an elevation of right ventricular pressure, alleviating right ventricular hypertrophy and the remodeling of pulmonary arterioles. This effect on the pulmonary vasculature is comparable with reports that AM inhibits the proliferation of cultured vascular smooth muscle cells isolated from rats or of those from human pulmonary artery (Kano et al., 1996; Upton et al 2001). Thus, AM seems to be a new therapeutic tool for treating patients with pulmonary hypertension; however, when infused intravenously, AM lowers not only pulmonary arterial pressure but also systemic blood pressure. In an attempt to avoid the effect on the systemic circulation, Nagaya et al. (2003) administered AM as an aerosol using an ultrasonic nebulizer in experimental pulmonary hypertension. Repeated inhalation effectively reduced pulmonary artery pressure and total pulmonary resistance, without affecting the systemic arterial pressure or heart rate. This novel approach seems promising for utilizing AM in the treatment of primary pulmonary hypertension, for which few effective medical treatments are currently available.

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