I am not an expert on the subject, nor do I smoke, but experts unequivocally tell me smoking increases stress after the high wears off. This is the Straight Dope, however, so a superficial argumentum ad verecundiam will not suffice!
I did some cursory research and from what I can tell nicotine is acutely correlated with cortisol[1][2][3][4][5], a product of stress. Correlation is not causation (unless we are talking about lax psychology), so I dug a little further.
It turns out scientists identify stress with actions of the hypothalamic-pituitary-adrenal (HPA) axis, a major neuroendocrine system. As the name suggests, this system consists of interactions between the hypothalamus (in your brain), the pituitary gland (also in your brain), and the adrenal glands (on top of each kidney). The basic idea is that together, the HPA axis produces stress in the physiological sense. It starts when the hypothalamus produces two peptides called arginine vasopressin (AVP) and corticotropin-releasing hormones (CRH).
AVP goes to the bloodstream and to other parts of the brain. From the bloodstream it binds to vassopressin receptor 2 (V2R) in the kidneys nephrons, which is coupled to G. Binding with V2R causes G activation of adenylate cyclase which increases cyclic adenosine monophosphate (cAMP) within the cell. cAMP in turn activates protein kinase A (PKA), which starts a chain reaction that makes these kidney cells absorb water passing through the kidney (urine) into the bloodstream[6]. This conserves water as part of the fight-or-flight response. Studies have measured increased AVP in smokers[7][8].
CRH goes straight to the pituitary gland. CRH ligands bind to corticotropin-releasing hormone receptor 1 (CRH-R1), which causes G activation of adenylyl cyclase which synthesizes cyclic adenosine monophosphate (cAMP)[9][10]. cAMP in turn activates PKA, which starts a chain reaction causes the secretion of a polypeptide tropic hormone called adrenocorticotropic hormone (ACTH) into the blood[11]. Studies also measured increased ACTH in smokers[1].
ACTH eventually reaches the zona fasciculata, part of the adrenal cortex within the adrenal glands. There it binds to melanocortin 2 (MC2) receptors, which leads to G activation of adenylyl cyclase which synthesize cAMP. In these cells, increased cAMP activates PKA, which starts a chain reaction that secretes a glucocorticoid called cortisol, mentioned above[12]. You may know of hydrocortisone, which the same molecule in medicine form. Cortisol stimulates gluconeogenesis (blood sugar for fight-or-flight), suppresses the immune system, increases metabolism, and decreases bone formation. It also inhibits production of AVP and CRH to complete the negative feedback loop; and so sort of turns itself off.
For a nice little picture of the whole process, see this diagram from Professor Richard Bowen at Colorado State University:
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/acth.gif
So how exactly does nicotine affect the HPA axis?
In a 1984 study they gave some men enough cigarettes to induce nausea, then measured cortisol and ACTH. Nauseated men had higher levels than non-nauseated men. They concluded that smoking-induced nausea stimulates cortisol release by stimulating ACTH secretion, although it is unclear from that study what causes non-nauseated smokers cortisol levels to rise[13].
A study with habitual male smokers compared cortisol levels after a night of abstinence plus either average or denicotinized cigarettes, and found the nicotine to cause the increase of cortisol[14].
Researchers incubated tiny slices of rat kidneys with nicotine. They found increased production of cyclic adenosine monophosphate (cAMP) in the pituitary gland. As explained above, cAMP in certain pituitary gland cells activates PKA and produces cortisol. Coupled with elevated cortisol observed in smokers, the researchers concluded nicotine induces increased generation of cAMP, which in turn mediates cortisol production through the processes described above[15].
Put all of this together and you have the scientific consensus that smoking causes stress[16].
[1] Baer L., & Radichevich I. (1985). Cigarette smoking in hypertensive patients. Blood pressure and endocrine responses. The American Journal of Medicine, 78(4), 564-568. Redirecting
[2] Szostak-Wegierek D., Björntorp P., Mårin P., Lindstedt G., & Andersson B. (1996). Influence of Smoking on Hormone Secretion in Obese and Lean Female Smokers. Obesity Research, 4(4), 321-328. https://doi.org/10.1002/j.1550-8528.1996.tb00239.x
[3] Chiodera P., Volpi R., Capretti L., Speroni G., Necchi-Ghiri S., Caffarri G., Colla R., & Coiro V. (1997). Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus. Clinical Endocrinology, 46(3), 351-357. https://doi.org/10.1046/j.1365-2265.1997.1470945.x
[4] Steptoe A., & Ussher M. (2006). Smoking, cortisol and nicotine. International Journal of Psychophysiology, 59(3), 228-235. Redirecting
[5] Badrick A., Kirschbaum C., & Kumari M. (2007). The Relationship between Smoking Status and Cortisol Secretion. The Journal of Clinical Endocrinology & Metabolism, 92(3), 819-824. Relationship between Smoking Status and Cortisol Secretion | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic
[6] Boone M., & Deen P. M. T. (2008). Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption. Pflugers Archiv: European Journal of Physiology, 456(6). 1005-1024. Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption | Pflügers Archiv - European Journal of Physiology
[7] Pomerleau O. F., Fertig J. B., Seyler L. E., & Jaffe J. (1983). Neuroendocrine reactivity to nicotine in smokers. Psychopharmacology, 81(1), 61-67. Neuroendocrine reactivity to nicotine in smokers | Psychopharmacology
[8] Waeber B., Schaller J., Nussberger J., Bussien P., Hofbauer K. G., & Brunner H. R. (1984). Skin blood flow reduction induced by cigarette smoking: role of vasopressin. American Journal of Physiology: Heart and Circulatory Physiology, 247(6), H895-H901. https://doi.org/10.1152/ajpheart.1984.247.6.H895
[9] Millan M. A., Samra A. A., Wynn P. C., Catt K. J., & Aguilera G. (1987). Receptors and Actions of Corticotropin-Releasing Hormone in the Primate Pituitary Gland. The Journal of Clinical Endocrinology & Metabolism, 64(5), 1036-1041. Receptors and Actions of Corticotropin-Releasing Hormone in the Primate Pituitary Gland | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic
[10] Hillhouse E. W., & Grammatopoulos D. K. (2006). The Molecular Mechanisms Underlying the Regulation of the Biological Activity of Corticotropin-Releasing Hormone Receptors: Implications for Physiology and Pathophysiology. Endocrine Reviews, 27(3), 260-286. https://doi.org/10.1210/er.2005-0034
[11] Kuryshev Y. A., Childs G. V., & Ritchie A.K. (1995). Corticotropin-releasing hormone stimulation of Ca2+ entry in corticotropes is partially dependent on protein kinase A. Endocrinology, 136(9), 3925-3935. https://doi.org/10.1210/endo.136.9.7649101
[12] Margioris A., & Tsatsanis, C. (2016). ACTH Action on the Adrenals. Endotext. Retrieved from ACTH Action on the Adrenals - Endotext - NCBI Bookshelf (Original work published 2000).
[13] Seyler L. E. Jr, Fertig J., Pomerleau O., Hunt D., & Parker K. (1984). The effects of smoking on ACTH and cortisol secretion. Life Sciences, 34(1), 57-65. Redirecting
[14] Xue Y., Morris M., Ni L., Guthrie S. K., Zubieta J. K., Gonzalez K., McConnell D. S., & Domino E. F. (2010). Venous plasma nicotine correlates of hormonal effects of tobacco smoking. Pharmacology Biochemistry and Behavior, 95(2), 209-215. Redirecting
[15] Gossain V. V., Sherma N. K., Srivastava L., Michelakis A. M., & Rovner D. R. (1986). Hormonal Effects of Smoking—II: Effects on Plasma Cortisol, Growth Hormone, and Prolactin. The American Journal of the Medical Sciences, 291(5), 325-327. Redirecting
[16] Tweed J. O., Hsia S. H., Lufty K., & Friedman T. (2012). Trends in Endocrinology & Metabolism, 23(7), 334-342. Redirecting