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Hypertension (HTN) is a chronic disease that has become a growing public health problem in countries around the world, including Pakistan. Successful HTN control is an essential cornerstone in the prevention of morbidity and mortality associated with uncontrolled HTN. However, patients’ beliefs about their disease, treatment and control are related to the outcome of successful HTN control and management. Likewise, doctors’ understanding of HTN and its treatment is equally important and can affect their practice and HTN management. There is little qualitative research considering patients’ and doctors’ understanding of HTN, its treatment and how it influences HTN management in Pakistan. Therefore, the current study aimed to elicit patients’ and doctors’ perceptions, attitudes and beliefs about HTN and its treatment in urban areas of Pakistan. A qualitative study that drew on grounded theory principles was undertaken in two public hospitals of Pakistan. Thirty in-depth semi-structured interviews with hypertensive patients and thirty interviews with doctors were conducted in two hospitals. Interviews were translated and transcribed from Urdu into English and NVivo was used to organise the data in a systematic way. Data were analysed using a constant comparative approach based on the principles of grounded theory. The study revealed that patients’ (n=30) beliefs were complex, deep-rooted and influenced their attitude towards HTN treatment. Patients’ beliefs were informed by understanding gleaned from the socio-cultural environment (local norms, social relations, religion), individual factors (e.g. income, co-morbidities) and interactions with doctors. In contrast, doctors’ (n=30) own understandings on what constitutes successful HTN management often contradicted patients’ beliefs. Doctors’ reported that time restraints and work burden affected their approach to treatment and the provision of information to patients. Findings also revealed an overlap between patients’ and doctors’ beliefs, however, in relation to adopting lifestyle changes for management of HTN. In general, though doctors paid less consideration to patients’ beliefs in routine clinical practice and evaluated patients through the filter of their own beliefs. The findings suggest that doctors could provide a better service care by aligning with their patients on a common understanding about HTN management and providing culturally appropriate information. Doctors should be aware of the understanding hypertensive patients attach to HTN and avoid providing treatment based on their own beliefs. Doctors must engage with patients’ beliefs and identify their particular healthcare needs in order to achieve control of HTN in Pakistan.

The enhanced platelet activity in hypertension has been suggested to contribute to the increased risk of cardiovascular disease in this condition. Various antihypertensive drugs have been examined both in vitro and in vivo for their ability to inhibit platelet activation. Antihypertensive drugs which possess selective [alpha]1-adrenoceptor blocking activity, e.g. prazosin, doxazosin and urapidil, have been found to inhibit platelet aggregation in some studies. Naftopidil is a new [alpha]1-adrenoceptor blocker but its effects on platelet function have not yet been studied. The main objective of the present study, therefore, was to study the effects of naftopidil in comparison with doxazosin on human platelet aggregation and secretory responses in vitro. The effects of the calcium channel blocker nifedipine were also investigated for comparative purposes. When platelet aggregation was induced by individual agonists, naftopidil but not doxazosin caused slight inhibitions of adrenaline- and serotonin- induced aggregation. Both drugs, however, failed to inhibit aggregation induced by ADP and collagen. Moreover, naftopidil markedly and, to a lesser extent, doxazosin inhibited the aggregation induced by sub-threshold concentrations of adrenaline in combination with sub-threshold concentrations of ADP, collagen or serotonin. In a washed platelet system naftopidil and, to a lesser extent, doxazosin inhibited adrenaline-induced aggregation. In the same system, naftopidil inhibited partially collagen-induced platelet aggregation. Naftopidil and doxazosin also inhibited the release of the a-granular component, platelet-derived growth factor, induced by adrenaline but not that induced by collagen. In the presence of naftopidil and doxazosin apparent increases in platelet serotonin release were observed possibly indicating that these drugs block the uptake mechanism for serotonin in platelets. Nifedipine was found to inhibit collagen-induced platelet aggregation and release of serotonin but it did not inhibit the release of PDGF. In order to clarify the modes of action of naftopidil, doxazosin and nifedipine as inhibitors of platelet activation, their effects on platelet signal transduction mechanisms were studied in washed platelets. Naftopidil and doxazosin inhibited the mobilization of intra platelet calcium induced by collagen and adrenaline. Naftopidil but not doxazosin inhibited adrenaline- and collagen-induced TXB2 generation. The platelet cyclic AMP, which mediates platelet inhibition, was not affected by either naftopidil or doxazosin. However, both drugs prevented the decline in platelet cyclic AMP stimulated by adrenaline. In comparison with naftopidil and doxazosin, nifedipine produced a greater inhibition of collagen-induced calcium mobilization and also inhibited the collagen- induced TXB2 production, comparable in its extent to that produced by naftopidil. Overall, it is concluded that naftopidil and, to a lesser extent, doxazosin inhibit platelet activation, possibly through antagonistic actions on platelet [alpha]2-adrenoceptors and suppressant effects on stimulus-induced calcium mobilization. Experiments with specific [alpha]2-adrenoceptor antagonists will be necessary to establish this mode of action. Moreover, the inhibitory action of naftopidil on TXA2 generation may contribute to its marked inhibition of adrenaline-induced platelet activation which is believed to be dependent on the formation of cyclooxygenase metabolites.